97 results on '"Jilani, K."'
Search Results
2. Comparison of surface enhanced Raman spectroscopy and Raman spectroscopy for the detection of breast cancer based on serum samples
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Nargis, H.F., Nawaz, H., Bhatti, H.N., Jilani, K., and Saleem, M.
- Published
- 2021
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3. A new approach of photocatalytic degradation of remazol brilliant blue by environment friendly fabricated zinc oxide nanoparticle
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Bibi, I., Kamal, S., Abbas, Z., Atta, S., Majid, F., Jilani, K., Hussain, A. I., Kamal, A., Nouren, S., and Abbas, A.
- Published
- 2020
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4. Raman spectroscopy of blood plasma samples from breast cancer patients at different stages
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Nargis, H.F., Nawaz, H., Ditta, A., Mahmood, T., Majeed, M.I., Rashid, N., Muddassar, M., Bhatti, H.N., Saleem, M., Jilani, K., Bonnier, F., and Byrne, H.J.
- Published
- 2019
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5. Electron acoustic solitons in magneto-rotating electron-positron-ion plasma with nonthermal electrons and positrons
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Jilani, K., Mirza, Arshad M., and Iqbal, J.
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- 2015
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6. Electrostatic electron acoustic solitons in electron-positron-ion plasma with superthermal electrons and positrons
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Jilani, K., Mirza, Arshad M., and Khan, Tufail A.
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- 2014
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7. Ion-acoustic solitons in pair-ion plasma with non-thermal electrons
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Jilani, K., Mirza, Arshad M., and Khan, Tufail A.
- Published
- 2013
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8. A new approach of photocatalytic degradation of remazol brilliant blue by environment friendly fabricated zinc oxide nanoparticle
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Bibi, I., primary, Kamal, S., additional, Abbas, Z., additional, Atta, S., additional, Majid, F., additional, Jilani, K., additional, Hussain, A. I., additional, Kamal, A., additional, Nouren, S., additional, and Abbas, A., additional
- Published
- 2019
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9. Erythrocyte phospholipid scrambling and cell swelling induced by CORM-2
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Tripodi, P. M., Rosaclerio, L., Jilani, K., Lang, E., Qadri, S. M., Zelenak, C., Schleicher, E., Faggio, Caterina, and Lang, F.
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Red blood cell ,Red blood cell, CORM-2,apoptosis ,apoptosis ,CORM-2 - Published
- 2012
10. Tanshinone IIA stimulates erythrocyte phosphatidylserine exposure
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Rosaclerio, L., Tripodi, P. M., Zelenak, C., Qadri, S. M., Jilani, K., Faggio, Caterina, and Lang, F.
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Tanshinone ,cell volume regulation ,red blood cell ,eryptosis - Published
- 2011
11. Effect of cold plasma permittivity on the radiation of the dominant TEM-wave by an impedance loaded parallel-plate waveguide radiator
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Ayub, M., primary, Khan, Tufail A., additional, and Jilani, K., additional
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- 2015
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12. E-polarized plane wave diffraction by an impedance loaded parallel-plate waveguide located in cold plasma
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Khan, Tufail A, primary, Ayub, M, additional, and Jilani, K, additional
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- 2014
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13. Tanshinone IIA stimulates erythrocyte phosphatidylserine exposure
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Zelenak, C., Pasham, V., Jilani, K., Tripodi, P.M., Rosaclerio, L., Pathare, G.T., Lupescu, A., Faggio, C., Qadri, S.M., Lang, F., Zelenak, C., Pasham, V., Jilani, K., Tripodi, P.M., Rosaclerio, L., Pathare, G.T., Lupescu, A., Faggio, C., Qadri, S.M., and Lang, F.
- Abstract
Contains fulltext : 109681.pdf (publisher's version ) (Open Access), Tanshinone IIA, an antimicrobial, antioxidant, antianaphylactic, antifibrotic, vasodilating, antiatherosclerotic, organo-protective and antineoplastic component from the rhizome of Salvia miltiorrhiza, is known to trigger apoptosis of tumor cells. Tanshinone IIA is effective in part through mitochondrial depolarization and altered gene expression. Erythrocytes lack mitochondria and nuclei but may undergo eryptosis, an apoptosis-like suicidal cell death characterized by cell shrinkage and cell membrane scrambling with phosphatidylserine exposure at the cell surface. Eryptosis is triggered by increase of cytosolic Ca(2+) activity, ATP depletion and ceramide formation. The present study explored, whether tanshinone IIA elicits eryptosis. Cytosolic Ca(2+)-concentration was determined from Fluo3-fluorescence, cell volume from forward scatter, phosphatidylserine exposure from binding of fluorescent annexin V, hemolysis from hemoglobin concentration in the supernatant, ATP concentration utilizing luciferin-luciferase and ceramide formation utilizing fluorescent anticeramide antibodies. Clearance of circulating erythrocytes was estimated by CFSE-labeling. A 48 h exposure to tanshinone IIA (>/=10 microM) significantly increased cytosolic Ca(2+)-concentration, decreased ATP concentration (25 microM), increased lactate concentration (25 microM), increased ceramide formation (25 microM), decreased forward scatter, increased annexin-V-binding and increased (albeit to a much smaller extent) hemolysis. The effect of 25 microM tanshinone IIA on annexin-V binding was partially reversed in the nominal absence of Ca(2+). Labelled tanshinone IIA-treated erythrocytes were more rapidly cleared from the circulating blood in comparison to untreated erythrocytes. The present observations reveal a completely novel effect of tanshinone IIA, i.e. triggering of Ca(2+) entry, ATP depletion and ceramide formation in erythrocytes, events eventually leading to eryptosis with cell shrinkage and cell
- Published
- 2012
14. Electrostatic electron acoustic solitons in electron-positron-ion plasma with superthermal electrons and positrons
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Jilani, K., primary, Mirza, Arshad M., additional, and Khan, Tufail A., additional
- Published
- 2013
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15. Effect of cold plasma permittivity on the radiation of the dominant TEM-wave by an impedance loaded parallel-plate waveguide radiator.
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Ayub, M., Khan, Tufail A., and Jilani, K.
- Subjects
RADIATORS ,WAVEGUIDES ,ELECTROMAGNETIC waves ,LOW temperature plasmas ,TRANSMISSION electron microscopy ,ARTIFICIAL satellites - Abstract
The effects of wall impedances on the radiation of the dominant transverse electromagnetic wave by an impedance loaded parallel-plate waveguide radiator immersed in a cold plasma have been analyzed. The solution to the governing mathematical model in cold plasma is determined while using the Wiener-Hopf technique. It is observed that the amplitude of the radiated field increases with increasing permittivity of the plasma. Thework presentedmay be of great interest to quantify the effects of ionosphere plasma on the communicating signals between Earth station and an artificial satellite in the Earth's atmosphere. [ABSTRACT FROM AUTHOR]
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- 2016
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16. Ion-acoustic solitons in pair-ion plasma with non-thermal electrons
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Jilani, K., primary, Mirza, Arshad M., additional, and Khan, Tufail A., additional
- Published
- 2012
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17. Optimization of a mobile robot's path tracking.
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Hayet, T., M'sirdi Nacer, K., and Jilani, K.
- Published
- 2011
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18. Levofloxacin induces erythrocyte contraction leading to red cell death.
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Aslam HM, Sohail A, Shahid A, Khan MAB, Sharif MU, Kausar R, Nawab S, Farooq W, Jilani K, and Rasheed M
- Abstract
Background: Levofloxacin, a fluoroquinolone, is an extensively used antibiotic effective against both positively and negatively staining bacteria. It works by inhibiting bacterial topoisomerase type II and topoisomerase type IV, resulting in impaired DNA synthesis and bacterial cell death. Eryptosis is another term for apoptotic cell death of erythrocyte marked by cell shrinkage, phosphatidylserine (PS) flipping, and membrane blebbing., Methods: The intent of the present research was to look at the eryptotic effect of levofloxacin by exposing erythrocytes to therapeutical doses (7, 14 µM) of levofloxacin for 48 hours. Cell size evaluation, PS subjection to outside, and calcium channel inhibition were carried out to investigate eryptosis. Oxidative stress generated by levofloxacin was measured as a putative mechanism of eryptosis using glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase activities. Similarly, hemolysis measurements demonstrated levofloxacin's cytotoxic effect., Results: Our findings showed that therapeutic doses of levofloxacin can cause a considerable decline in antioxidant enzymes activities, as well as induce cell shrinkage, PS externalization, and hemolysis in erythrocytes. The role of calcium in triggering erythrocyte shrinkage was also confirmed., Conclusion: In conclusion, our findings showed that the indicated levofloxacin doses caused oxidative stress, which leads to erythrocyte death via eryptosis and hemolysis. These findings emphasize the importance of using levofloxacin with caution and the need for additional research to mitigate these side effects., Competing Interests: Conflict of interest: The authors declare no conflict of interest., (© 2024 The Authors.)
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- 2024
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19. NiO/MnFe 2 O 4 Nanocomposite Photoluminescence, Structural, Morphological, Magnetic, and Optical Properties: Photocatalytic Removal of Cresol Red under Visible Light Irradiation.
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Amjad M, Bibi I, Majid F, Jilani K, Sultan M, Raza Q, Ghafoor A, Alwadai N, Nazir A, and Iqbal M
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In this study, pure nickel oxide (NiO), manganese ferrite (MnFe
2 O4 or MFO), and binary nickel oxide/manganese ferrite (NiO/MFO1-4) nanocomposites (NCs) were synthesized using the Sol-Gel method. A comprehensive investigation into their photoluminescence, structural, morphological, magnetic, optical, and photocatalytic properties was conducted. Raman analysis, UV-Vis spectroscopy, Fourier-transform infrared spectroscopy, scanning electron microscopy, and X-ray diffraction techniques were used to characterize the materials. The synthesized samples exhibited superparamagnetic behavior, as revealed by our analysis of their magnetic properties. A lower recombination rate was shown by the photoluminescence analysis, which is helpful for raising photocatalytic activity. The photocatalytic activity was evaluated for the degradation of Cresol Red (CR) dye. 91.6% of CR dye was degraded by NiO/MFO-4 nanocomposite, and the NC dosage as well as solution pH affected the photocatalytic performance significantly. In four sequential photocatalytic cycles, the magnetically separable NCs were stable and recyclable. The enhanced photocatalytic activity and magnetic separability revealed the potential application of NiO/MFO-4 as an efficient photocatalyst for the removal of dyes from industrial wastewater under solar light irradiation., Competing Interests: The authors declare no competing financial interest., (© 2024 The Authors. Published by American Chemical Society.)- Published
- 2024
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20. Antibacterial, Antibiofilm, and Anti-Quorum Sensing Potential of Novel Synthetic Compounds Against Pathogenic Bacteria Isolated From Chronic Sinusitis Patients.
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Rafiq MA, Shahid M, Jilani K, and Aslam MA
- Abstract
Quorum sensing (QS) is a major controller of virulence and biofilm formation in pathogenic bacteria. The aim of the research was to screen novel synthetic compounds (18) from 2 series (Pyrazole and Diene dione) for quorum sensing and biofilm inhibitory potential against resistant pathogens isolated from patients with chronic sinusitis. Most of the compounds have documented zone of inhibition against Gram positive strains Staphylococcus aureus , Enterococcus faecalis and moderate activity against Gram negative Klebseilla pneumoniae and Proteus mirabilis in comparison with standard antibiotic. Compounds Q1 and Q7 have given the maximum zone of inhibition 18 and 20 mm with MICs 0.312 mg/mL and .156 mg/mL against S aureus and E faecalis, respectively. Some compounds were equally potent at inhibiting the formation of biofilm which later established by phase contrast microscopy. Regarding quorum sensing inhibition, the tested concentration of synthetic compound UA3 0.313 mg/mL inhibited violacein production without decreasing Chromobacterium pseudoviolaceum count which was significantly lower than determined MIC's. It was depicted from the results that selected compounds exhibited low level of cytotoxicity toward human red blood cells. Hence, these findings revealed that most novel compounds were effective antibacterial, whereas compound UA3 has shared significant anti-quorum sensing potential against Chromobacterium pseudoviolaceum., Competing Interests: The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article., (© The Author(s) 2022.)
- Published
- 2022
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21. Pathogenic role of cytokines in COVID-19, its association with contributing co-morbidities and possible therapeutic regimens.
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Tanveer A, Akhtar B, Sharif A, Saleem U, Rasul A, Ahmad A, and Jilani K
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- Bronchodilator Agents therapeutic use, Comorbidity, Cytokine Release Syndrome drug therapy, Cytokines, Humans, SARS-CoV-2, Inflammatory Bowel Diseases, Pulmonary Disease, Chronic Obstructive drug therapy, COVID-19 Drug Treatment
- Abstract
The Covid-19, a threatening pandemic, was originated from China in December 2019 and spread quickly to all over the world. The pathogenesis of coronavirus is linked with the disproportionate response of the immune system. This involves the systemic inflammatory reaction which is characterized by marked pro-inflammatory cytokine release commonly known as cytokine release storm (CRS). The pro inflammatory cytokines are involved in cascade of pulmonary inflammation, hyper coagulation and thrombosis which may be lethal for the individual. That's why, it is very important to have understanding of pro inflammatory cytokines and their pathological role in SARS-CoV-2. The pathogenesis of Covid is not the same in every individual, it can vary due to the presence of pre-existing comorbidities like suffering from already an inflammatory disease such as rheumatoid arthritis (RA), inflammatory bowel disease (IBD), chronic obstructive pulmonary disease (COPD), an immune-compromised patients suffering from Diabetes Mellitus (DM) and Tuberculosis (TB) are more vulnerable morbidity and complications following COVID-19. This review is particularly related to COVID-19 patients having comorbidity of other inflammatory diseases. We have discussed the brief pathogenesis of COVID-19 and cytokines release storm with reference to other co-morbidities including RA, IBD, COPD, DM and TB. The available therapeutic regimens for COVID-19 including cytokine inhibitors, anti-viral, anti-biotic, bronchodilators, JAK- inhibitors, immunomodulators and anti-fibrotic agents have also been discussed briefly. Moreover, newly emerging medicines in the clinical trials have also been discussed which are found to be effective in treating Covid-19., (© 2022. The Author(s), under exclusive licence to Springer Nature Switzerland AG.)
- Published
- 2022
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22. Induction of Erythrocyte Membrane Blebbing by Methotrexate-Induced Oxidative Stress.
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Sattar T, Jilani K, Parveen K, Mushataq Z, Nawaz H, and Khan MAB
- Abstract
Methotrexate (MTX) is a common chemotherapeutical agent and folate antagonist with reported apoptotic activity in nucleated cells. The presented research work was planned to investigate the eryptotic effects of methotrexate after the exposure of erythrocytes to therapeutical doses (10-15 μM) of methotrexate. Eryptosis and the role of calcium in the stimulation of membrane blebbing were evaluated through the determination of mean cell volume. Oxidative stress induced by methotrexate (10-15 μM) was determined by antioxidative enzyme activities. Cytotoxic activity against human erythrocytes was examined through hemolysis assay. Exposure of erythrocytes to methotrexate results in significant reduction of superoxide dismutase, catalase, and superoxide dismutase activities at 10 and 15 μM in comparison to the untreated cells. Erythrocytes mean cell volume (MCV) was increased after 48 hours exposure of erythrocytes to methotrexate (10 μM). Significantly increased hemolysis percentage was observed at 10 μM after 48 hours incubation of erythrocytes with methotrexate. The results of the study suggested that the therapeutical doses (10-15 μM) of methotrexate may lead to increase in eryptotic and hemolytic activity of erythrocytes through free radical generation and subsequent calcium entry., Competing Interests: Declaration of Conflicting Interests: The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article., (© The Author(s) 2022.)
- Published
- 2022
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23. Stimulation of Erythrocyte Membrane Blebbing by Bifenthrin Induced Oxidative Stress.
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Mukhtar F, Jilani K, Bibi I, Mushataq Z, Bari Khan MA, and Fatima M
- Abstract
Background: Bifenthrin is an insecticide and anti-estrogenic compound primarily used to control residential pests by depolarizing sodium gated voltage channels in the nervous system. Eryptosis, the suicidal death of erythrocytes, featured by PS exposure, membrane blebbing and cell shrinkage. Anemia is an outcome of uncontrolled eryptosis., Research Design: In this study, erythrocytes were treated with different concentrations (.5-1-1.5 μM) of bifenthrin over a period of 48 hours. In order to investigate the oxidative stress induced by bifenthrin, catalase, superoxide dismutase, and glutathione peroxidase activities were investigated., Results: Obtained data indicated the decrease in the enzymes (superoxide dismutase, glutathione peroxidase, and catalase) activities in bifenthrin treated cells at 1 μM concentration. In addition, measurement of cell size and confirmation of the role of calcium in the stimulation of the eryptotic activity of bifenthrin were performed. A significant increase in mean cell volume was found in the presence of bifenthrin and a decrease in mean cell volume in the presence of calcium channel blocker was observed. Similarly, there was also a significant increase in the percentage of hemolysis indicating the necrotic activity of bifenthrin., Conclusions: It is concluded that the indicated doses of bifenthrin triggered oxidative stress which may lead to early cell death by eryptosis and hemolysis., Competing Interests: Declaration of Conflicting Interests: The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article., (© The Author(s) 2022.)
- Published
- 2022
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24. The electrochemical, dielectric, and ferroelectric properties of Gd and Fe doped LaNiO 3 with an efficient solar-light driven catalytic activity to oxidize malachite green dye.
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Iqbal S, Bibi I, Majid F, Jilani K, Kamal S, Iqbal M, Ata S, Nazar N, Albalawi H, and Alwadai N
- Subjects
- Catalysis, X-Ray Diffraction, Light, Rosaniline Dyes
- Abstract
This work investigates the effects of double ion substitution on the ferroelectric, electrochemical, dielectric and photocatalytic properties of Gd and Fe doped La
1-y Gdy Ni1-x Fex O3 nanoparticles (NPs). La1-y Gdy Ni1-x Fex O3 was fabricated by facile micro-emulsion path and its properties were studied by thermogravimetric analysis (TGA), X-ray diffraction (XRD), scanning electron microscopy (SEM), Raman scattering, Fourier Transform of Infrared (FTIR), energy dispersive x-rays (EDX) techniques. It has a distorted rhombohedral shape with crystallite size within the range of 17-23 nm. The doped material has a spherical heterogeneous morphology, and its surface area increased with increased doping. The electrochemical (CV, EIS, and I-V), conductivity and dielectric (dielectric constant and low dielectric & tangent loss) properties of La1-y Gdy Ni1-x Fex O3 were dependent on the contents of the dopants (Gd and Fe). The doped material had improved specific capacitance compared to the undoped LaNiO3 due to the synergistic effect of Gd and Fe on the doped materials. The conductivity of Gd and Fe doped LaNiO3 5.16 × 104 Sm-1 was enhanced compared to the undoped LaNiO3 3.52 × 10-2 Sm1 . Furthermore, hysteresis loop was used to investigate the coercivity (Hc), saturation magnetization (Ms) and remanence (Mr) of the material. The Ms and Mr values were enhanced with the content of the dopants. The photocatalytic activity (PCA) of the material in degrading malachite green (MG) dye was studied. La1-y Gdy Ni1-x Fex O3 NPs was able to degrade up to 96.4% of the dye under visible light irradiation in 50 min. La1-y Gdy Ni1-x Fex O3 has remarkable dielectric, electrochemical, ferroelectric and photo-catalytic properties and have potential applications in microwave, electrical, electronic, energy storage devices. It is also an active photo-catalyst material for the removal/oxidation of toxic pollutants from the environment., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2021 Elsevier Inc. All rights reserved.)- Published
- 2022
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25. Induction of Erythrocyte Shrinkage by Omeprazole.
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Naveed A, Jilani K, Siddique AB, Akbar M, Riaz M, Mushtaq Z, Sikandar M, Ilyas S, Bibi I, Asghar A, Rasool G, and Irfan M
- Abstract
Omeprazole, a proton pump inhibitor blocks the H
+ /K+ -ATPase channels of gastric parietal cells. It is used for the treatment of peptic ulcer. Prolonged use of omeprazole may involve in inducing anemia. The key marker of eryptosis includes membrane blebbing, cell shrinkage and phosphatidylserine (PS) exposure at the cell surface. In current study, the eryptotic, oxidative as well as hemolytic effects of therapeutical doses (0.5, 1 and 1.5 µM) of omeprazole were investigated after exposing erythrocytes for 48 hours. Investigation of eryptosis was done by cell size measurement, PS exposure determination and calcium channel inhibition. As a possible mechanism of omeprazole induced eryptosis, oxidative stress was investigated by determining the catalase, glutathione peroxidase and superoxide dismutase activities. Similarly, necrotic effect of omeprazole on erythrocytes was also evaluated through hemolysis measurement. Results of our study illustrated that 1.5 µM of omeprazole may induce significant decrease in superoxide dismutase, glutathione peroxidase and catalase activities as well as triggered the erythrocytes shrinkage, PS exposure and hemolysis. Role of calcium was also confirmed in inducing erythrocyte shrinkage. It is concluded that the exposure of erythrocytes with 1.5 µM omeprazole may enhance the rate of eryptosis and hemolysis by inducing oxidative stress., Competing Interests: Declaration of Conflicting Interests: The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article., (© The Author(s) 2020.)- Published
- 2020
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26. Stimulation of Erythrocyte Membrane Blebbing by Naproxen Sodium.
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Ilyas S, Jilani K, Sikandar M, Siddiq S, Riaz M, Naveed A, Bibi I, Nawaz H, Irfan M, and Asghar A
- Abstract
Naproxen sodium is a nonsteroidal anti-inflammatory drug (NSAID) having antipyretic and analgesic properties, mainly used for the treatment of rheumatoid arthritis and osteoarthritis. Eryptosis is an alternative term used for suicidal erythrocyte death. In the current study, eryptotic effect of naproxen sodium characterized by membrane blebbing was investigated in erythrocytes after 48 hours of treatment with different concentrations (1-25 µM). The experimental work related to investigation of eryptosis was done by cell size measurement and confirmation of calcium role in the induction of membrane blebbing. As a possible mechanism of eryptosis, oxidative stress induced by naproxen sodium was determined by catalase, glutathione peroxidase, and superoxide dismutase activities. Similarly, hemolytic effect of naproxen sodium was also determined by hemolysis measurement. Results of our study illustrated that the therapeutic doses (10-25 µM) of naproxen sodium induce oxidative stress, confirmed by significant decrease in superoxide dismutase, catalase, and glutathione peroxidase activities that lead to the triggering of cell death by eryptosis and hemolysis., Competing Interests: Declaration of Conflicting Interests: The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article., (© The Author(s) 2020.)
- Published
- 2020
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27. Atorvastatin Induced Erythrocytes Membrane Blebbing.
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Rana RB, Jilani K, Shahid M, Riaz M, Ranjha MH, Bibi I, Asghar A, and Irfan M
- Abstract
Atorvastatin, an inhibitor of 3-hydroxy-3-methylglutaryl-coenzymeA reductase, is usually used for the treatment of hypercholesterolemia. Besides its pharmacological and side actions, its toxic effects on human nucleus devoid of erythrocytes are still unknown. Eryptosis is an alternative term used for suicidal erythrocyte death. Membrane blebbing is among the common markers of eryptosis. In this study, eryptotic effect of atorvastatin was investigated by exposing the erythrocytes for 48 hours to different concentrations (1-10 µM) of atorvastatin. The experimental work related to investigation of eryptosis was done by cell size measurement and calcium channel inhibition. As a possible mechanism of eryptosis, atorvastatin-induced oxidative stress was evaluated by determining catalase, glutathione peroxidase, and superoxide dismutase activities. Similarly, necrotic effect of atorvastatin was also determined by hemolytic assay. Results of our study illustrated that the tested doses of atorvastatin may induce oxidative stress as observed by significant reduction in superoxide dismutase, glutathione peroxidase, and catalase activities as well as induce eryptosis, featured by erythrocytes membrane blebbing. The study concluded that induction of oxidative stress by atorvastatin may lead to eryptosis., Competing Interests: Declaration of Conflicting Interests: The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
- Published
- 2019
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28. Cu nanoparticles synthesis using biological molecule of P. granatum seeds extract as reducing and capping agent: Growth mechanism and photo-catalytic activity.
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Nazar N, Bibi I, Kamal S, Iqbal M, Nouren S, Jilani K, Umair M, and Ata S
- Subjects
- Catalysis drug effects, Green Chemistry Technology, Metal Nanoparticles ultrastructure, Plant Extracts chemical synthesis, Plant Extracts pharmacology, Seeds chemistry, Copper chemistry, Metal Nanoparticles chemistry, Photochemical Processes drug effects, Plant Extracts chemistry
- Abstract
In view of extended applications of nanoparticles, the nanoparticles synthesis is an extensive research field and green synthesis is one of the co-friendly methodologies. Plant extract mediated synthesis of nanoparticles has gained much attention in current decade. In current investigation, copper nanoparticles (CuNPs) were prepared using P. granatum seeds extract (biological molecules) from copper(II) chloride salt. The synthesized CuNPs were characterized by UV-vis spectroscopy, X-ray diffraction measurements (XRD), scanning electron microscopy (SEM), Energy Dispersive X- Ray Spectroscopy (EDX), Fourier transform infra-red spectroscopy (FTIR) and atomic force microscopy techniques. The CuNPs formation occurred through reduction of metal ions followed by nucleation. The size of the CuNPs was in the range of 40-80nm (average particle size was 43.9nm) with semi spherical shape and uniformly distribution. Photocatalytic activity was evaluated by degrading methylene blue dye (150mg/L) at various CuNPs doses (10mg/L-100mg/L). The synthesized CuNPs showed excellent PCA for the degradation of methylene blue (MB) under solar light irradiation and up to 87.11% degradation was achieved. The oxidative degradation mechanism for MB was proposed. In view of efficient PCA, the use of biological molecules of P. granatum seeds extracts for the synthesis of CuNPs., (Copyright © 2017 Elsevier B.V. All rights reserved.)
- Published
- 2018
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29. Nickel nanoparticle synthesis using Camellia Sinensis as reducing and capping agent: Growth mechanism and photo-catalytic activity evaluation.
- Author
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Bibi I, Kamal S, Ahmed A, Iqbal M, Nouren S, Jilani K, Nazar N, Amir M, Abbas A, Ata S, and Majid F
- Subjects
- Catalysis, Chemistry Techniques, Synthetic, Oxidation-Reduction, Plant Leaves chemistry, Camellia sinensis chemistry, Metal Nanoparticles chemistry, Nanotechnology, Nickel chemistry, Photochemical Processes, Plant Extracts chemistry
- Abstract
Recently, the biosynthesis of nanoparticle attracted the attention of scientific community due to its simplicity, ease and eco-friendly nature. In the present study, Camellia Sinensis (C. Sinensis) leaves extract was employed for the synthesis of nickel nanoparticles (NiNPs). The fabricated NiNPs were characterized by scanning electron microscopy (SEM) and energy-dispersive X-ray (EDX) and X-ray diffraction techniques. The photocatalytic activity (PCA) was evaluated by degrading crystal violet (CV) dye. The NiNPs size was in the range of 43.87-48.76nm, spherical in shape and uniformly distributed with magnetization saturation of 0.073 emu/g. The NiNPs showed promising PCA under solar light irradiation. At optimized conditions, up to 99.5% CV dye degradation was achieved. Results revealed that biosynthesis can be adopted for the synthesis of NiNPs in nano-size range since it is simple, cost effective and eco-friendly in nature versus physico-chemical methods., (Copyright © 2017. Published by Elsevier B.V.)
- Published
- 2017
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30. Frequency and the risk factors of hepatitis C virus in pregnant women; A hospital based descriptive study in Gadap Town Karachi.
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Jilani K, Zulfiqar B, Memon QB, and Fahim MF
- Abstract
Objective: To determine the frequency and the risk factors of hepatitis C virus in pregnant women at Al-Tibri Medical College & Hospital in Gadap Town Karachi., Methods: This was a descriptive cross sectional study conducted at Obstetrics & Gynecology OPD of Al-Tibri Medical College & Hospital, Isra University Karachi Campus from 10
th June to 10th September 2016. A total of 400 pregnant women of 16-45 years of age, who came in outpatient department for antenatal checkup were selected for the study. The diagnosed cases of Hepatitis C were excluded from the study. Detailed history including age, parity, risk factor like history of transfusion, previous surgeries, vaginal deliveries was taken and relevant examination was performed. Patients on routine antenatal investigation if found to have Anti HCV positive on Immunochromatography Test (ICT) method were further confirmed by Elisa. A well designed proforma was used for data collection., Results: During the period of 3 months 400 women in antenatal clinic were tested for hepatitis C, out of which 27 (6.6%) were positive for HCV antibodies. The age of the women included ranges from 16-45 years. Thirteen (7.9%) pregnant women having HCV +ve antibodies fell in 26-30 years of age group. From 27 HCV +ve patients, 19 (70.3%) were multigravida & 8 (29.6%) were primigravida. Majority of the patients (77%) had history of injections., Conclusion: There is high prevalence of Hepatitis C infection among pregnant female in our setup. The possible risk factors are injection, blood transfusion and surgery.- Published
- 2017
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31. Accelerated apoptotic death and in vivo turnover of erythrocytes in mice lacking functional mitogen- and stress-activated kinase MSK1/2.
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Lang E, Bissinger R, Fajol A, Salker MS, Singh Y, Zelenak C, Ghashghaeinia M, Gu S, Jilani K, Lupescu A, Reyskens KM, Ackermann TF, Föller M, Schleicher E, Sheffield WP, Arthur JS, Lang F, and Qadri SM
- Subjects
- Animals, Erythrocyte Indices, Erythrocytes pathology, Female, Gene Expression, Hematocrit, Hemoglobins, Hemolysis, Humans, Male, Mice, Mice, Knockout, Osmotic Fragility, Osmotic Pressure, Phosphatidylserines metabolism, Primary Cell Culture, Reticulocyte Count, Ribosomal Protein S6 Kinases, 90-kDa deficiency, Apoptosis genetics, Erythrocytes metabolism, Ribosomal Protein S6 Kinases, 90-kDa genetics
- Abstract
The mitogen- and stress-activated kinase MSK1/2 plays a decisive role in apoptosis. In analogy to apoptosis of nucleated cells, suicidal erythrocyte death called eryptosis is characterized by cell shrinkage and cell membrane scrambling leading to phosphatidylserine (PS) externalization. Here, we explored whether MSK1/2 participates in the regulation of eryptosis. To this end, erythrocytes were isolated from mice lacking functional MSK1/2 (msk(-/-)) and corresponding wild-type mice (msk(+/+)). Blood count, hematocrit, hemoglobin concentration and mean erythrocyte volume were similar in both msk(-/-) and msk(+/+) mice, but reticulocyte count was significantly increased in msk(-/-) mice. Cell membrane PS exposure was similar in untreated msk(-/-) and msk(+/+) erythrocytes, but was enhanced by pathophysiological cell stressors ex vivo such as hyperosmotic shock or energy depletion to significantly higher levels in msk(-/-) erythrocytes than in msk(+/+) erythrocytes. Cell shrinkage following hyperosmotic shock and energy depletion, as well as hemolysis following decrease of extracellular osmolarity was more pronounced in msk(-/-) erythrocytes. The in vivo clearance of autologously-infused CFSE-labeled erythrocytes from circulating blood was faster in msk(-/-) mice. The spleens from msk(-/-) mice contained a significantly greater number of PS-exposing erythrocytes than spleens from msk(+/+) mice. The present observations point to accelerated eryptosis and subsequent clearance of erythrocytes leading to enhanced erythrocyte turnover in MSK1/2-deficient mice.
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- 2015
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32. Enhanced eryptosis following juglone exposure.
- Author
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Calabrò S, Alzoubi K, Bissinger R, Jilani K, Faggio C, and Lang F
- Subjects
- Adenosine Triphosphate blood, Annexin A5 metabolism, Calcium blood, Cell Size drug effects, Ceramides blood, Erythrocytes metabolism, Humans, In Vitro Techniques, Phosphatidylserines blood, Antineoplastic Agents, Phytogenic toxicity, Apoptosis drug effects, Erythrocytes drug effects, Naphthoquinones toxicity
- Abstract
Juglone, a quinone isolated from Juglans mandshurica Maxim, has previously been shown to be effective against malignancy. The effect is at least partially due to stimulation of suicidal death or apoptosis of tumour cells. On the other hand, juglone has been shown to counteract apoptosis, for example, of neurons. In analogy to apoptosis of nucleated cells, erythrocytes may enter eryptosis, a suicidal death characterized by cell shrinkage and breakdown of phosphatidylserine asymmetry of the cell membrane with phosphatidylserine exposure at the erythrocyte surface. Stimulators of eryptosis include increase in cytosolic Ca(2+) activity [(Ca(2+) )i]. This study explored whether juglone stimulates eryptosis. To this end, erythrocyte volume was estimated from forward scatter, phosphatidylserine exposure at the erythrocyte surface from FITC annexin V binding, ceramide abundance from binding of fluorescent antibodies in flow cytometry and cytosolic ATP with a luciferin-luciferase-based assay. As a result, a 24-hr exposure of human erythrocytes to juglone (5 μM) significantly decreased erythrocyte forward scatter. Juglone (1-5 μM) significantly increased the percentage of annexin V binding cells. Juglone (5 μM) significantly increased ceramide abundance at the erythrocyte surface and decreased erythrocyte ATP concentration. The effect of juglone (10 μM) on annexin V binding was slightly but significantly blunted by removal of extracellular Ca(2+) and by addition of protein kinase C (PKC) inhibitor staurosporine (1 μM). In conclusion, juglone stimulates suicidal erythrocyte death or eryptosis at least in part by upregulation of ceramide abundance, energy depletion and activation of PKC., (© 2014 Nordic Association for the Publication of BCPT (former Nordic Pharmacological Society).)
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- 2015
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33. Therapeutic potential of manipulating suicidal erythrocyte death.
- Author
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Lang F, Jilani K, and Lang E
- Subjects
- Anemia etiology, Anemia pathology, Animals, Apoptosis drug effects, Drug Design, Erythrocytes physiology, Humans, Malaria parasitology, Oxidative Stress physiology, Phagocytes metabolism, Anemia drug therapy, Erythrocytes drug effects, Malaria drug therapy
- Abstract
Introduction: Eryptosis, the suicidal erythrocyte death, is characterized by erythrocyte shrinkage and phosphatidylserine translocation to the erythrocyte surface. Eryptosis is triggered by cell stress such as energy depletion and oxidative stress, by Ca(2+)-entry, ceramide, caspases, calpain and/or altered activity of several kinases. Phosphatidylserine-exposing erythrocytes adhere to the vascular wall and may thus impede microcirculation. Eryptotic cells are further engulfed by phagocytes and thus rapidly cleared from circulation., Areas Covered: Stimulation of eryptosis contributes to anemia of several clinical conditions such as metabolic syndrome, diabetes, malignancy, hepatic failure, heart failure, uremia, hemolytic uremic syndrome, sepsis, fever, dehydration, mycoplasma infection, malaria, iron deficiency, sickle cell anemia, thalassemia, glucose-6-phosphate dehydrogenase deficiency and Wilson's disease. On the other hand, eryptosis with subsequent clearance of infected erythrocytes in malaria may counteract parasitemia., Expert Opinion: In theory, anemia due to excessive eryptosis could be alleviated by treatment with small molecules inhibiting eryptosis. In malaria, stimulators of eryptosis may accelerate death of infected erythrocytes and thus favorably influence the clinical course of the disease. Many small molecules inhibit or stimulate eryptosis. Several stimulators favorably influence murine malaria. Further preclinical and subsequent clinical studies are required to elucidate the therapeutic potential of stimulators or inhibitors of eryptosis.
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- 2015
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34. Vitamin D-Rich Diet in Mice Modulates Erythrocyte Survival.
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Lang E, Jilani K, Bissinger R, Rexhepaj R, Zelenak C, Lupescu A, Lang F, and Qadri SM
- Subjects
- Animals, Blood Cell Count, Calcium metabolism, Cell Size drug effects, Diet, Erythrocyte Membrane drug effects, Erythropoietin metabolism, Female, Mice, Mice, Inbred C57BL, Osmotic Pressure drug effects, Phosphatidylserines blood, Erythrocyte Aging drug effects, Vitamin D therapeutic use, Vitamins therapeutic use
- Abstract
Background/aims: Epidemiological evidence suggests that vitamin D deficiency is associated with anemia. The potent metabolite 1,25(OH)2 vitamin D3 [1,25(OH)2D3] activates various signaling cascades regulating a myriad of cellular functions including suicidal cell death or apoptosis. Suicidal death of erythrocytes or eryptosis is characterized by cell shrinkage and cell membrane scrambling leading to phosphatidylserine (PS) externalization. Stimulation of eryptosis may limit lifespan of circulating erythrocytes and thus cause anemia. In the present study, we explored the effect of a high vitamin D diet (10,000 I.U. vitamin D for 14 days) in mice on eryptosis., Methods: Plasma concentrations of erythropoietin were estimated using an immunoassay kit, blood count using an electronic hematology particle counter, relative reticulocyte numbers using Retic-COUNT® reagent, PS exposure at the cell surface from annexin V binding, cell volume from forward scatter, and cytosolic Ca(2+) ([Ca(2+)]i) from Fluo3-fluorescence in FACS analysis., Results: Vitamin D treatment decreased mean corpuscular volume, reticulocyte count, and plasma erythropoietin levels. Vitamin D treatment slightly but significantly decreased forward scatter but did not significantly modify spontaneous PS exposure and [Ca(2+)]i of freshly drawn erythrocytes. Vitamin D treatment augmented the stimulation of PS exposure and cell shrinkage following exposure to hyperosmotic shock (addition of 550 mM sucrose) or energy depletion (glucose removal) without significantly modifying [Ca(2+)]i., Conclusions: The present observations point to a subtle effect of exogenous vitamin D supplementation on erythrocyte survival., (© 2015 S. Karger AG, Basel.)
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- 2015
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35. The Role of Janus Kinase 3 in the Regulation of Na⁺/K⁺ ATPase under Energy Depletion.
- Author
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Hosseinzadeh Z, Honisch S, Schmid E, Jilani K, Szteyn K, Bhavsar S, Singh Y, Palmada M, Umbach AT, Shumilina E, and Lang F
- Subjects
- 2,4-Dinitrophenol pharmacology, Animals, Cells, Cultured, Dendritic Cells drug effects, Dendritic Cells metabolism, Energy Metabolism drug effects, Female, Gene Deletion, Janus Kinase 3 antagonists & inhibitors, Janus Kinase 3 genetics, Male, Mice, Mutation, Oocytes drug effects, Oocytes metabolism, Quinazolines pharmacology, Xenopus, Adenosine Triphosphate metabolism, Janus Kinase 3 metabolism, Sodium-Potassium-Exchanging ATPase metabolism
- Abstract
Background/aims: Janus kinase-3 (JAK3) is activated during energy depletion. Energy-consuming pumps include the Na(+)/K(+)-ATPase. The present study explored whether JAK3 regulates Na(+)/K(+)-ATPase in dendritic cells (DCs)., Methods: Ouabain (100 µM)-sensitive (Iouabain) and K(+)-induced (Ipump) outward currents were determined by utilizing whole cell patch-clamp, Na(+)/K(+)-ATPase α1-subunit mRNA levels by RT-PCR, Na(+)/K(+)-ATPase protein abundance by flow cytometry or immunofluorescence, and cellular ATP by luciferase-assay in DCs from bone marrow of JAK3-knockout (jak3(-/-)) or wild-type mice (jak3(+/+)). Ipump was further determined by voltage clamp in Xenopus oocytes expressing JAK3, active (A568V)JAK3 or inactive (K851A)JAK3., Results: Na(+)/K(+)-ATPase α1-subunit mRNA and protein levels, as well as Ipump and Iouabain were significantly higher in jak3(-/-)DCs than in jak3(+/+)DCs. Energy depletion by 4h pre-treatment with 2,4-dinitro-phenol significantly decreased Ipump in jak3(+/+) DCs but not in jak3(-/-)DCs. Cellular ATP was significantly lower in jak3(-/-)DCs than in jak3(+/+)DCs and decreased in both genotypes by 2,4-dinitro-phenol, an effect significantly more pronounced in jak3(-/-)DCs than in jak3(+/+)DCs and strongly blunted by ouabain in both jak3(+/+) and jak3(-/-)DCs. Ipump and Iouabain in oocytes were decreased by expression of JAK3 and of (A568V)JAK3 but not of (K851A)JAK3. JAK3 inhibitor WHI-P154 (4-[(3'-bromo-4'-hydroxyphenyl)amino]-6,7-dimethoxyquinazoline, 22 μM) enhanced Ipump and Iouabain in JAK3 expressing oocytes. The difference between (A568V)JAK3 and (K851A)JAK3 expressing oocytes was virtually abrogated by actinomycin D (50 nM)., Conclusions: JAK3 down-regulates Na(+)/K(+)-ATPase activity, an effect involving gene expression and profoundly curtailing ATP consumption., (© 2015 S. Karger AG, Basel.)
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- 2015
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36. Stimulation of erythrocyte cell membrane scrambling by nystatin.
- Author
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Malik A, Bissinger R, Jilani K, and Lang F
- Subjects
- Annexin A5 metabolism, Apoptosis drug effects, Calcium metabolism, Cell Size drug effects, Erythrocyte Membrane metabolism, Erythrocytes cytology, Erythrocytes drug effects, Flow Cytometry, Humans, Phosphatidylserines metabolism, Potassium metabolism, Sodium metabolism, Antifungal Agents pharmacology, Erythrocyte Membrane drug effects, Nystatin pharmacology
- Abstract
The antifungal ionophore nystatin dissipates the Na(+) and K(+) gradients across the cell membrane, leading to cellular gain of Na(+) and cellular loss of K(+) . The increase of cellular Na(+) concentration may result in Ca(2+) accumulation in exchange for Na(+) . Increase of cytosolic Ca(2+) activity ([Ca(2+) ]i ) and loss of cellular K(+) foster apoptosis-like suicidal erythrocyte death or eryptosis, which is characterised by cell shrinkage and cell membrane scrambling leading to phosphatidylserine exposure at the erythrocyte surface. The present study explored whether nystatin stimulates eryptosis. Cell volume was estimated from forward scatter (FSC), phosphatidylserine exposure from annexin V binding and [Ca(2+) ]i from Fluo3-fluorescence in flow cytometry. A 48-hr exposure to nystatin (15 μg/ml) was followed by a significant increase of [Ca(2+) ]i , a significant increase of annexin V binding and a significant decrease of FSC. The annexin V binding after nystatin treatment was significantly blunted in the nominal absence of extracellular Ca(2+) . Partial replacement of extracellular Na(+) with extracellular K(+) blunted the nystatin-induced erythrocyte shrinkage but increased [Ca(2+) ]i and annexin V binding. Nystatin triggers cell membrane scrambling, an effect at least partially due to entry of extracellular Ca(2+) ., (© 2014 Nordic Association for the Publication of BCPT (former Nordic Pharmacological Society).)
- Published
- 2015
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37. Triggering of erythrocyte cell membrane scrambling by salinomycin.
- Author
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Bissinger R, Malik A, Jilani K, and Lang F
- Subjects
- Annexin A5 metabolism, Anti-Bacterial Agents administration & dosage, Anti-Bacterial Agents pharmacology, Calcium metabolism, Dose-Response Relationship, Drug, Erythrocyte Membrane metabolism, Erythrocytes metabolism, Hemolysis drug effects, Humans, Oxidative Stress drug effects, Pyrans administration & dosage, Erythrocyte Membrane drug effects, Erythrocytes drug effects, Phosphatidylserines metabolism, Pyrans pharmacology
- Abstract
Salinomycin, a polyether ionophore antibiotic effective against a variety of pathogens, has been shown to trigger apoptosis of cancer cells and cancer stem cells. The substance is thus considered for the treatment of malignancy. Salinomycin compromises tumour cell survival at least in part by interference with mitochondrial function. Erythrocytes lack mitochondria but may undergo apoptosis-like suicidal cell death or eryptosis, which is characterized by scrambling of the cell membrane with phosphatidylserine exposure at the erythrocyte surface. Signalling involved in the triggering of eryptosis includes activation of oxidant-sensitive Ca(2+) permeable cation channels with subsequent increase in cytosolic Ca(2+) activity ([Ca(2+)]i). This study explored whether salinomycin stimulates eryptosis. Phosphatidylserine-exposing erythrocytes were identified by measurement of annexin-V binding, cell volume was estimated from forward scatter, haemolysis determined from haemoglobin release, [Ca(2+)]i quantified utilizing Fluo3-fluorescence and oxidative stress from 2',7' dichlorodihydrofluorescein diacetate (DCFDA) fluorescence in flow cytometry. A 48-hr exposure to salinomycin (5-100 nM) was followed by a significant increase in Fluo3-fluorescence, DCFDA fluorescence and annexin-V binding, as well as a significant decrease in forward scatter (at 5-10 nM, but not at 50 and 100 nM). The annexin-V binding after salinomycin treatment was significantly blunted but not abrogated in the nominal absence of extracellular Ca(2+) or in the presence of antioxidant n-acetyl cysteine (1 mM). Salinomycin triggers cell membrane scrambling, an effect at least partially due to oxidative stress and entry of extracellular Ca(2+)., (© 2014 Nordic Association for the Publication of BCPT (former Nordic Pharmacological Society).)
- Published
- 2014
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38. Piperlongumine-induced phosphatidylserine translocation in the erythrocyte membrane.
- Author
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Bissinger R, Malik A, Warsi J, Jilani K, and Lang F
- Subjects
- Annexin A5 metabolism, Apoptosis drug effects, Calcium metabolism, Cell Membrane drug effects, Cell Membrane metabolism, Ceramides metabolism, Erythrocyte Membrane metabolism, Fluoresceins metabolism, Humans, Oxidative Stress drug effects, Reactive Oxygen Species metabolism, Dioxolanes pharmacology, Erythrocyte Membrane drug effects, Phosphatidylserines metabolism
- Abstract
Background: Piperlongumine, a component of Piper longum fruit, is considered as a treatment for malignancy. It is effective by inducing apoptosis. Mechanisms involved in the apoptotic action of piperlongumine include oxidative stress and activation of p38 kinase. In analogy to apoptosis of nucleated cells, erythrocytes may undergo eryptosis, the suicidal death of erythrocytes characterized by cell shrinkage and cell membrane scrambling with phosphatidylserine-exposure at the erythrocyte surface. Signaling involved in eryptosis include increase of cytosolic Ca²⁺-activity ([Ca²⁺]i), formation of ceramide, oxidative stress and activation of p38 kinase., Methods: Cell volume was estimated from forward scatter, phosphatidylserine-exposure from annexin V binding, [Ca²⁺]i from Fluo3 fluorescence, reactive oxygen species from 2',7'-dichlorodihydrofluorescein-diacetate fluorescence, and ceramide abundance from binding of fluorescent antibodies in flow cytometry., Results: A 48 h exposure to piperlongumine (30 µM) was followed by significant decrease of forward scatter and increase of annexin-V-binding. Piperlongumine did not significantly modify [Ca²⁺]i and the effect was not dependent on presence of extracellular Ca²⁺. Piperlongumine significantly increased ROS formation and ceramide abundance., Conclusions: Piperlongumine triggers cell membrane scrambling, an effect independent from entry of extracellular Ca²⁺ but at least partially due to ROS and ceramide formation.
- Published
- 2014
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39. In vitro sensitization of erythrocytes to programmed cell death following baicalein treatment.
- Author
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Bissinger R, Malik A, Honisch S, Warsi J, Jilani K, and Lang F
- Subjects
- Calcium metabolism, Cell Membrane drug effects, Cells, Cultured, Ceramides metabolism, Cytosol metabolism, Erythrocytes metabolism, Humans, Apoptosis drug effects, Erythrocytes drug effects, Flavanones pharmacology
- Abstract
The polyphenolic flavonoid Baicalein has been shown to trigger suicidal death or apoptosis of tumor cells and is thus considered for the prevention and treatment of malignancy. Similar to apoptosis of nucleated cells, erythrocytes may enter eryptosis, the suicidal erythrocyte death characterized by cell shrinkage and cell membrane scrambling with phosphatidylserine translocation to the erythrocyte surface. Stimulators of eryptosis include increase of cytosolic Ca2+-activity ([Ca2+]i) and ceramide. The present study explored whether Baicalein stimulates eryptosis. To this end, forward scatter was taken for measurement of cell volume, annexin-V-binding for phosphatidylserine-exposure, Fluo3 fluorescence for [Ca2+]i and fluorescent antibodies for ceramide abundance. As a result, a 48 h exposure of human erythrocytes to Baicalein was followed by significant decrease of forward scatter (≥10 µM), significant increase of the percentage of annexin-V-binding cells (≥25 µM), significant increase of [Ca2+]i (50 µM) and significant increase of ceramide abundance (50 µM). The effect of Baicalein (50 µM) on annexin-V-binding was significantly blunted but not abrogated by removal of extracellular Ca2+. In conclusion, at the concentrations employed, Baicalein stimulates suicidal erythrocyte death or eryptosis, an effect at least in part due to the combined effects of Ca2+ entry and ceramide formation.
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- 2014
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40. Upregulation of excitatory amino acid transporters by coexpression of Janus kinase 3.
- Author
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Warsi J, Luo D, Elvira B, Jilani K, Shumilina E, Hosseinzadeh Z, and Lang F
- Subjects
- Animals, Cell Proliferation, Mice, Mice, Knockout, Patch-Clamp Techniques, Up-Regulation, Xenopus laevis, Amino Acid Transport System X-AG metabolism, Glutamic Acid metabolism, Janus Kinase 3 physiology, Oocytes metabolism, Signal Transduction
- Abstract
Janus kinase 3 (JAK3) contributes to cytokine receptor signaling, confers cell survival and stimulates cell proliferation. The gain of function mutation JAK3(A572V) is found in acute megakaryoplastic leukemia. Replacement of ATP coordinating lysine by alanine yields inactive JAK3(K855A). Most recent observations revealed the capacity of JAK3 to regulate ion transport. This study thus explored whether JAK3 regulates glutamate transporters EAAT1-4, carriers accomplishing transport of glutamate and aspartate in a variety of cells including intestinal cells, renal cells, glial cells, and neurons. To this end, EAAT1, 2, 3, or 4 were expressed in Xenopus oocytes with or without additional expression of mouse wild-type JAK3, constitutively active JAK3(A568V) or inactive JAK3(K851A), and electrogenic glutamate transport was determined by dual electrode voltage clamp. Moreover, Ussing chamber was employed to determine electrogenic glutamate transport in intestine from mice lacking functional JAK3 (jak3(-/-)) and from corresponding wild-type mice (jak3(+/+)). As a result, in EAAT1, 2, 3, or 4 expressing oocytes, but not in oocytes injected with water, addition of glutamate to extracellular bath generated an inward current (Ig), which was significantly increased following coexpression of JAK3. Ig in oocytes expressing EAAT3 was further increased by JAK3(A568V) but not by JAK3(K851A). Ig in EAAT3 + JAK3 expressing oocytes was significantly decreased by JAK3 inhibitor WHI-P154 (22 µM). Kinetic analysis revealed that JAK3 increased maximal Ig and significantly reduced the glutamate concentration required for half maximal Ig (Km). Intestinal electrogenic glutamate transport was significantly lower in jak3(-/-) than in jak3(+/+) mice. In conclusion, JAK3 is a powerful regulator of excitatory amino acid transporter isoforms.
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- 2014
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41. In vitro induction of erythrocyte phosphatidylserine translocation by the natural naphthoquinone shikonin.
- Author
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Lupescu A, Bissinger R, Jilani K, and Lang F
- Subjects
- Adenosine Triphosphate blood, Biological Transport, Calcium blood, Erythrocytes metabolism, Humans, In Vitro Techniques, Erythrocytes drug effects, Naphthoquinones pharmacology, Phosphatidylserines blood
- Abstract
Shikonin, the most important component of Lithospermum erythrorhizon, has previously been shown to exert antioxidant, anti-inflammatory, antithrombotic, antiviral, antimicrobial and anticancer effects. The anticancer effect has been attributed to the stimulation of suicidal cell death or apoptosis. Similar to the apoptosis of nucleated cells, erythrocytes may experience eryptosis, the suicidal erythrocyte death characterized by cell shrinkage and by phosphatidylserine translocation to the erythrocyte surface. Triggers of eryptosis include the increase of cytosolic Ca2+-activity ([Ca2+]i) and ceramide formation. The present study explored whether Shikonin stimulates eryptosis. To this end, Fluo 3 fluorescence was measured to quantify [Ca2+]i, forward scatter to estimate cell volume, annexin V binding to identify phosphatidylserine-exposing erythrocytes, hemoglobin release to determine hemolysis and antibodies to quantify ceramide abundance. As a result, a 48 h exposure of human erythrocytes to Shikonin (1 µM) significantly increased [Ca2+]i, increased ceramide abundance, decreased forward scatter and increased annexin V binding. The effect of Shikonin (1 µM) on annexin V binding was significantly blunted, but not abolished by the removal of extracellular Ca2+. In conclusion, Shikonin stimulates suicidal erythrocyte death or eryptosis, an effect at least partially due to the stimulation of Ca2+ entry and ceramide formation.
- Published
- 2014
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42. Energy-sensitive regulation of Na+/K+-ATPase by Janus kinase 2.
- Author
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Bhavsar SK, Hosseinzadeh Z, Brenner D, Honisch S, Jilani K, Liu G, Szteyn K, Sopjani M, Mak TW, Shumilina E, and Lang F
- Subjects
- Adaptation, Physiological, Adenosine Triphosphate metabolism, Animals, Enzyme Activation, Humans, Janus Kinase 2 antagonists & inhibitors, Janus Kinase 2 genetics, Jurkat Cells, Membrane Potentials, Phosphorylation, Protein Kinase Inhibitors pharmacology, STAT5 Transcription Factor antagonists & inhibitors, STAT5 Transcription Factor metabolism, Signal Transduction, Sodium-Potassium-Exchanging ATPase genetics, Time Factors, Xenopus laevis, Energy Metabolism drug effects, Janus Kinase 2 metabolism, Sodium-Potassium-Exchanging ATPase metabolism
- Abstract
Janus kinase 2 (JAK2) contributes to intracellular signaling of leptin and erythropoietin, hormones protecting cells during energy depletion. The present study explores whether JAK2 is activated by energy depletion and regulates Na(+)/K(+)-ATPase, the major energy-consuming pump. In Jurkat cells, JAK2 activity was determined by radioactive kinase assay, phosphorylated JAK2 detected by Western blotting, ATP levels measured by luciferase assay, as well as Na(+)/K(+)-ATPase α1-subunit transcript and protein abundance determined by real-time PCR and Western blotting, respectively. Ouabain-sensitive K(+)-induced currents (Ipump) were measured by whole cell patch clamp. Ipump was further determined by dual-electrode voltage clamp in Xenopus oocytes injected with cRNA-encoding JAK2, active (V617F)JAK2, or inactive (K882E)JAK2. As a result, in Jurkat T cells, JAK2 activity significantly increased following energy depletion by sodium azide (NaN3) or 2,4- dinitro phenol (DNP). DNP- and NaN3-induced decrease of cellular ATP was significantly augmented by JAK2 inhibitor AG490 and blunted by Na(+)/K(+)-ATPase inhibitor ouabain. DNP decreased and AG490 enhanced Ipump as well as Na(+)/K(+)-ATPase α1-subunit transcript and protein abundance. The α1-subunit transcript levels were also enhanced by signal transducer and activator of transcription-5 inhibitor CAS 285986-31-4. In Xenopus oocytes, Ipump was significantly decreased by expression of JAK2 and (V617F)JAK2 but not of (K882E)JAK2, effects again reversed by AG490. In (V617F)JAK2-expressing Xenopus oocytes, neither DNP nor NaN3 resulted in further decline of Ipump. In Xenopus oocytes, the effect of (V617F)JAK2 on Ipump was not prevented by inhibition of transcription with actinomycin. In conclusion, JAK2 is a novel energy-sensing kinase that curtails energy consumption by downregulating Na(+)/K(+)-ATPase expression and activity.
- Published
- 2014
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43. Stimulation of erythrocyte cell membrane scrambling by gedunin.
- Author
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Lupescu A, Bissinger R, Warsi J, Jilani K, and Lang F
- Subjects
- Cell Death drug effects, Cell Size drug effects, Ceramides metabolism, Cytosol drug effects, Cytosol metabolism, Erythrocyte Membrane metabolism, Erythrocytes metabolism, Flow Cytometry, Humans, Limonins chemistry, Molecular Structure, Time Factors, Calcium metabolism, Erythrocyte Membrane drug effects, Erythrocytes drug effects, Limonins pharmacology, Phosphatidylserines metabolism
- Abstract
Background/aims: Gedunin, an inhibitor of heat shock protein HSP90, triggers apoptosis of tumor cells and is thus effective against malignancy. Moreover, the drug has antimalarial potency. In analogy to apoptosis of nucleated cells, erythrocytes may enter suicidal death or eryptosis, which is characterized by cell shrinkage and by phosphatidylserine translocation to the erythrocyte surface. Eryptosis may be triggered by increase of cytosolic Ca(2+)-activity ([Ca(2+)]i). The present study explored whether gedunin stimulates eryptosis., Methods: Forward scatter was determined to estimate cell volume, annexin V binding to identify phosphatidylserine-exposing erythrocytes, hemoglobin release to depict hemolysis, and Fluo3-fluorescence to quantify [Ca(2+)]i., Results: A 48 h exposure of human erythrocytes to gedunin significantly increased [Ca(2+)]i (12 µM), significantly decreased forward scatter (24 µM) and significantly increased annexin-V-binding (12 µM). The effect of gedunin (24 µM) on annexin-V-binding was virtually abrogated by removal of extracellular Ca(2+)., Conclusion: Gedunin stimulates suicidal erythrocyte death or eryptosis, an effect mainly if not exclusively due to stimulation of Ca(2+) entry., (© 2014 S. Karger AG, Basel.)
- Published
- 2014
- Full Text
- View/download PDF
44. Stimulation of erythrocyte death by phloretin.
- Author
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Bissinger R, Fischer S, Jilani K, and Lang F
- Subjects
- Annexin A5 metabolism, Apoptosis drug effects, Ceramides metabolism, Cytosol metabolism, Erythrocyte Membrane metabolism, Erythrocytes metabolism, Humans, Phosphatidylserines metabolism, p38 Mitogen-Activated Protein Kinases biosynthesis, Erythrocyte Membrane drug effects, Erythrocytes drug effects, Hemolysis drug effects, Phloretin administration & dosage
- Abstract
Background: Phloretin, a natural component of apples, pears and strawberries, has previously been shown to stimulate apoptosis of nucleated cells. Erythrocytes may similarly enter suicidal death or eryptosis, which is characterized by cell shrinkage and phospholipid scrambling of the erythrocyte cell membrane with phosphatidylserine translocation to the erythrocyte surface. Stimulators of eryptosis include increase of cytosolic Ca(2+)-activity ([Ca(2+)]i), ceramide, ATP depletion, and activation of protein kinase C (PKC) as well as p38 mitogen activated protein kinase (p38 kinase)., Methods: Phosphatidylserine exposure at the cell surface was estimated from annexin V binding, cell volume from forward scatter, [Ca(2+)]i from Fluo3-fluorescence, and ceramide abundance from binding of specific antibodies., Results: A 48 h exposure of human erythrocytes to phloretin significantly increased the percentage of annexin-V-binding cells (≥100 µM) without significantly influencing forward scatter. Phloretin did not significantly modify [Ca(2+)]i and the stimulation of annexin-V-binding by phloretin (300 µM) did not require presence of extracellular Ca(2+). Phloretin did not significantly modify erythrocyte ATP levels, and the effect of phloretin on annexin-V-binding was not significantly altered by PKC inhibitor staurosporine (1 µM) or p38 kinase inhibitor SB2203580 (2 µM). However, phloretin significantly increased the ceramide abundance at the cell surface., Conclusions: Phloretin stimulates phospholipid scrambling of the erythrocyte cell membrane, an effect at least partially due to up-regulation of ceramide abundance.
- Published
- 2014
- Full Text
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45. Stimulation of eryptosis by cryptotanshinone.
- Author
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Bissinger R, Lupescu A, Zelenak C, Jilani K, and Lang F
- Subjects
- Annexin A5 metabolism, Erythrocytes metabolism, Flow Cytometry, Humans, Apoptosis drug effects, Erythrocytes drug effects, Phenanthrenes pharmacology
- Abstract
Background/aims: Cryptotanshinone, a component of Salvia miltiorrhiza Bunge roots, may trigger suicidal death or apoptosis of tumor cells and has thus been recommended for the prevention and treatment of malignancy. On the other hand, Cryptotanshinone has been shown to counteract apoptosis of neurons and hepatocytes. Similar to apoptosis of nucleated cells, erythrocytes may enter eryptosis, a suicidal death characterized by cell shrinkage and phosphatidylserine translocation to the erythrocyte surface. Eryptosis may be triggered by increase of cytosolic Ca(2+)-activity ([Ca(2+)]i). The present study explored whether Cryptotanshinone stimulates eryptosis., Methods: Forward scatter was taken as measure of cell volume, annexin V binding for identification of phosphatidylserine-exposing erythrocytes and Fluo3-fluorescence for determination of [Ca(2+)]i., Results: A 48 h exposure of human erythrocytes to Cryptotanshinone (10 µM) was followed by significant decrease of forward scatter, significant increase of the percentage annexin-V-binding cells and significant increase of [Ca(2+)]i. The effect of Cryptotanshinone (1 µM) on annexin-V-binding was virtually abrogated by removal of extracellular Ca(2+)., Conclusion: Cryptotanshinone is a powerful stimulator of suicidal erythrocyte death or eryptosis, which is effective mainly, if not exclusively, by stimulation of Ca(2+) entry., (© 2014 S. Karger AG, Basel.)
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- 2014
- Full Text
- View/download PDF
46. Aristolochic acid induced suicidal erythrocyte death.
- Author
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Malik A, Bissinger R, Calabrò S, Faggio C, Jilani K, and Lang F
- Subjects
- Cell Death drug effects, Cell Death physiology, Cell Size drug effects, Dose-Response Relationship, Drug, Humans, Aristolochic Acids toxicity, Erythrocytes drug effects, Erythrocytes physiology
- Abstract
Background/aims: Aristolochic Acid, a component of Aristolochia plants, has been shown to cause acute kidney injury, renal aristolochic acid nephropathy, Balkan endemic nephropathy, and urothelial carcinoma. Aristolochic acid nephropathy may be associated with severe anemia. The anemia could theoretically be due to stimulation of eryptosis, the suicidal death of erythrocytes characterized by cell shrinkage and cell membrane scrambling with translocation of phosphatidylserine to the erythrocyte cell membrane surface. Signalling involved in the stimulation of eryptosis include increase of cytosolic Ca(2+)-activity ([Ca(2+)]i) and formation of ceramide., Methods: Cell volume was estimated from forward scatter, phosphatidylserine-exposure from annexin V binding, [Ca(2+)]i from Fluo3 fluorescence, and ceramide abundance from binding of fluorescent antibodies in flow cytometry., Results: A 48 hours exposure to Aristolochic Acid (≥ 75 µg/ml) was followed by a significant decrease of forward scatter and increase of annexin-V-binding. The effects were paralleled by a significant increase of [Ca(2+)]i and significantly blunted, but not abrogated by removal of extracellular Ca(2+). Aristolochic Acid further significantly increased ceramide abundance., Conclusions: Aristolochic Acid triggers eryptosis, an effect at least in part due to entry of extracellular Ca(2+) and ceramide formation., (© 2014 S. Karger AG, Basel.)
- Published
- 2014
- Full Text
- View/download PDF
47. Induction of suicidal erythrocyte death by novobiocin.
- Author
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Lupescu A, Bissinger R, Herrmann T, Oswald G, Jilani K, and Lang F
- Subjects
- Cell Death drug effects, Erythrocytes cytology, Humans, Annexin A5 metabolism, Calcium metabolism, Calcium Signaling drug effects, Ceramides metabolism, Erythrocytes metabolism, Novobiocin pharmacology
- Abstract
Background: Novobiocin, an aminocoumarin antibiotic, interferes with heat shock protein 90 and hypoxia inducible factor dependent gene expression and thus compromises cell survival. Similar to survival of nucleated cells, erythrocyte survival could be disrupted by eryptosis, the suicidal erythrocyte death characterized by cell shrinkage and by phospholipd scrambling of the cell membrane with phosphatidylserine translocation to the erythrocyte surface. Triggers of eryptosis include increase of cytosolic Ca(2+)-activity ([Ca(2+)]i). The Ca(2+) sensitivity of phospholipid scrambling is enhanced by ceramide. The present study explored, whether novobiocin elicits eryptosis., Methods: [Ca(2+)]i was estimated from Fluo3-fluorescence, ceramide abundance utilizing fluorescent antibodies, cell volume from forward scatter, phosphatidylserine-exposure from annexin V binding., Results: A 48 hours exposure to novobiocin (500 µM) was followed by a significant increase of [Ca(2+)]i, decrease of forward scatter, increase of annexin-V-binding and enhanced ceramide formation. Removal of extracellular Ca(2+) virtually abrogated the increase of annexin-V-binding following novobiocin exposure., Conclusions: Novobiocin stimulates eryptosis, an effect at least in part due to entry of extracellular Ca(2+) and formation of ceramide., (© 2014 S. Karger AG, Basel.)
- Published
- 2014
- Full Text
- View/download PDF
48. Ca(2+)-dependent suicidal erythrocyte death following zearalenone exposure.
- Author
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Jilani K and Lang F
- Subjects
- Annexin A5 metabolism, Cell Size drug effects, Erythrocytes metabolism, Hemoglobins metabolism, Hemolysis drug effects, Humans, Phosphatidylserines metabolism, Apoptosis drug effects, Calcium metabolism, Erythrocytes drug effects, Zearalenone toxicity
- Abstract
Zearalenone, a cereal mycotoxin with mycoestrogen activity and effect on fertility, is known to trigger apoptosis of a variety of nucleated cell types including hematopoietic progenitor cells. In analogy to apoptosis of nucleated cells, eryptosis, the suicidal death of erythrocytes, leads to cell shrinkage and cell membrane scrambling with phosphatidylserine exposure at the erythrocyte surface. The most important stimulator of eryptosis is an increase in cytosolic Ca(2+) activity ([Ca(2+)]i). The present study explored whether zearalenone triggers eryptosis. Erythrocyte volume was estimated from forward scatter, phosphatidylserine exposure at the erythrocyte surface from annexin-V binding, hemolysis from hemoglobin release, and [Ca(2+)]i from Fluo3 fluorescence. A 48-h exposure to zearalenone (≥25 μM) was followed by a significant increase in [Ca(2+)]i and annexin-V binding, and a significant decrease in forward scatter. The effect on annexin-V binding was significantly blunted in the nominal absence of extracellular Ca(2+). Zearalenone stimulates the suicidal erythrocyte death, an effect at least partially due to stimulation of Ca(2+) entry.
- Published
- 2013
- Full Text
- View/download PDF
49. Triggering of suicidal erythrocyte death by celecoxib.
- Author
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Lupescu A, Bissinger R, Jilani K, and Lang F
- Subjects
- Apoptosis drug effects, Calcium metabolism, Celecoxib, Cell Size drug effects, Cells, Cultured, Erythrocytes metabolism, Erythrocytes pathology, Hemolysis drug effects, Humans, Phosphatidylserines metabolism, Cyclooxygenase 2 Inhibitors pharmacology, Erythrocytes drug effects, Pyrazoles pharmacology, Sulfonamides pharmacology
- Abstract
The selective cyclooxygenase-2 (COX-2) inhibitor celecoxib triggers apoptosis of tumor cells and is thus effective against malignancy. The substance is at least partially effective through mitochondrial depolarization. Even though lacking mitochondria, erythrocytes may enter apoptosis-like suicidal death or eryptosis, which is characterized by cell shrinkage and by phosphatidylserine translocation to the erythrocyte surface. Eryptosis may be triggered by increase of cytosolic Ca2+-activity ([Ca2+]i). The present study explored whether celecoxib stimulates eryptosis. Forward scatter was determined to estimate cell volume, annexin V binding to identify phosphatidylserine-exposing erythrocytes, hemoglobin release to depict hemolysis, and Fluo3-fluorescence to quantify [Ca2+]i. A 48 h exposure of human erythrocytes to celecoxib was followed by significant increase of [Ca2+]i (15 µM), significant decrease of forward scatter (15 µM) and significant increase of annexin-V-binding (10 µM). Celecoxib (15 µM) induced annexin-V-binding was blunted but not abrogated by removal of extracellular Ca2+. In conclusion, celecoxib stimulates suicidal erythrocyte death or eryptosis, an effect partially due to stimulation of Ca2+ entry.
- Published
- 2013
- Full Text
- View/download PDF
50. Effect of honokiol on erythrocytes.
- Author
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Zbidah M, Lupescu A, Herrmann T, Yang W, Foller M, Jilani K, and Lang F
- Subjects
- Calcium metabolism, Cell Death drug effects, Cell Size drug effects, Cells, Cultured, Erythrocytes metabolism, Erythrocytes pathology, Hemolysis drug effects, Humans, Phosphatidylserines metabolism, Biphenyl Compounds toxicity, Erythrocytes drug effects, Lignans toxicity
- Abstract
Honokiol ((3,5-di-(2-propenyl)-1,1-biphenyl-2,2-diol), a component of Magnolia officinalis, stimulates apoptosis and is thus considered for the treatment of malignancy. In analogy to apoptosis of nucleated cells, erythrocytes may enter eryptosis, a suicidal death characterized by cell shrinkage and by breakdown of cell membrane phosphatidylserine asymmetry with phosphatidylserine-exposure at the erythrocyte surface. Eryptosis may be triggered following increase of cytosolic Ca(2+)-activity ([Ca(2+)]i). The present study explored, whether honokiol elicits eryptosis. Cell volume has been estimated from forward scatter, phosphatidylserine-exposure from annexin V binding, hemolysis from hemoglobin release, [Ca(2+)]i from Fluo3-fluorescence, and ceramide from fluorescent antibodies. As a result, a 48 h exposure to honokiol was followed by a slight but significant increase of [Ca(2+)]i (15 μM), significant decrease of forward scatter (5 μM), significant increase of annexin-V-binding (5 μM) and significant increase of ceramide formation (15 μM). Honokiol further induced slight, but significant hemolysis. Honokiol (15 μM) induced annexin-V-binding was significantly blunted but not abrogated in the nominal absence of extracellular Ca(2+). In conclusion, honokiol triggers suicidal erythrocyte death or eryptosis, an effect at least in part due to stimulation of Ca(2+) entry and ceramide formation., (Copyright © 2013 Elsevier Ltd. All rights reserved.)
- Published
- 2013
- Full Text
- View/download PDF
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