Search

Your search keyword '"Riganti, C."' showing total 447 results
Start Over Author "Riganti, C."
447 results on '"Riganti, C."'

5. Tuning of surface chemical and optical properties of nanodiamonds for biosensing and drug delivery applications

Author

Aprà, Pietro, primary, Arpicco, S., additional, Bincoletto, V., additional, Bernardi, E., additional, Moreva, E., additional, Genovese, M., additional, Kopecka, J., additional, Losero, E., additional, Mino, L., additional, Olivero, P., additional, Riganti, C., additional, Stella, C., additional, Sturari, S., additional, Traina, P., additional, Varzi, V., additional, Zanelli, G., additional, and Picollo, F., additional

Published
2023
Full Text
View/download PDF

6. Treatment with ROS detoxifying gold quantum clusters alleviates the functional decline in a mouse model of Friedreich ataxia

Author

Villa, C, Legato, M, Umbach, A, Riganti, C, Jones, R, Martini, B, Boido, M, Medana, C, Facchinetti, I, Barni, D, Pinto, M, Arguello, T, Belicchi, M, Fagiolari, G, Liaci, C, Moggio, M, Ruffo, R, Moraes, C, Monguzzi, A, Merlo, G, Torrente, Y, Villa C., Legato M., Umbach A., Riganti C., Jones R., Martini B., Boido M., Medana C., Facchinetti I., Barni D., Pinto M., Arguello T., Belicchi M., Fagiolari G., Liaci C., Moggio M., Ruffo R., Moraes C. T., Monguzzi A., Merlo G. R., Torrente Y., Villa, C, Legato, M, Umbach, A, Riganti, C, Jones, R, Martini, B, Boido, M, Medana, C, Facchinetti, I, Barni, D, Pinto, M, Arguello, T, Belicchi, M, Fagiolari, G, Liaci, C, Moggio, M, Ruffo, R, Moraes, C, Monguzzi, A, Merlo, G, Torrente, Y, Villa C., Legato M., Umbach A., Riganti C., Jones R., Martini B., Boido M., Medana C., Facchinetti I., Barni D., Pinto M., Arguello T., Belicchi M., Fagiolari G., Liaci C., Moggio M., Ruffo R., Moraes C. T., Monguzzi A., Merlo G. R., and Torrente Y.

Abstract

Friedreich ataxia (FRDA) is caused by the reduced expression of the mitochondrial protein frataxin (FXN) due to an intronic GAA trinucleotide repeat expansion in the FXN gene. Although FRDA has no cure and few treatment options, there is research dedicated to finding an agent that can curb disease progression and address symptoms as neurobehavioral deficits, muscle endurance, and heart contractile dysfunctions. Because oxidative stress and mitochondrial dysfunctions are implicated in FRDA, we demonstrated the systemic delivery of catalysts activity of gold cluster superstructures (Au8-pXs) to improve cell response to mitochondrial reactive oxygen species and thereby alleviate FRDA-related pathology in mesenchymal stem cells from patients with FRDA. We also found that systemic injection of Au8-pXs ameliorated motor function and cardiac contractility of YG8sR mouse model that recapitulates the FRDA phenotype. These effects were associated to long-term improvement of mitochondrial functions and antioxidant cell responses. We related these events to an increased expression of frataxin, which was sustained by reduced autophagy. Overall, these results encourage further optimization of Au8-pXs in experimental clinical strategies for the treatment of FRDA.

Published
2021

8. Hazards assessment of micro- and nanoplastics and associated additives/contaminants to human health

Author

Katsumiti, Alberto, Rodríguez-Llopis, Isabel, Boland, S, Devineau, S, Miremont, D, Ramsperger, A.F.R.M, Löder, MGJ, Laforsch, C, Drobne, D, Michelini, S, Repar, N, Hoekstra, L, Duivenvoorde, L, van der Zande, M, Tamargo, A, Di Maira, G, Tedesco, E, Benetti, F, Antonello, G, Fenoglio, I, Riganti, C, Bergamaschi, E, Jacobsen, N.R, Kazour, M, Peijnenburg, W, Kühnel, D, Haugen, Ø. P, Wallin, H, Narui, S, and Afanou, A.J.K

Subjects
hazard assessment, microplastics, exposure, toxicity, human health, nanoplastics, plastic particles
Abstract

Summary of objectives, test materials, target systems,strategies, and expected outcomes of Work Package 3 of the PlasticsFatE Project PlasticsFatE has received funding from the European Union’s Horizon 2020 Research and Innovation programme, under the Grant Agreement number 965367

Published
2022
Full Text
View/download PDF

12. Sdox, a H2S releasing anthracycline, with a safer profile than doxorubicin toward vasculature

Author

Durante, M., Frosini, M., Chiaino, E., Fusi, F., Gamberucci, A., Gorelli, B., Chegaev, K., Riganti, C., and Saponara, S.

Subjects
Pharmacology, Myocytes, Physiology, A7r5 cells, Doxorubicin, EA.hy926 cells, Rat aorta ring, Vascular toxicity, Muscle, Smooth, Vascular, Myocytes, Smooth Muscle, Anthracyclines, Antibiotics, Antineoplastic, Antineoplastic, Smooth Muscle, Antibiotics, Vascular, Molecular Medicine, Muscle, Smooth
Published
2022

14. Transcriptional perturbation of protein arginine methyltransferase-5 exhibits MTAP-selective oncosuppression

Author

Busacca, S, Zhang, Q, Sharkey, A, Dawson, AG, Moore, DA, Waller, DA, Nakas, A, Jones, C, Cain, K, Luo, J-L, Salcedo, A, Salaroglio, IC, Riganti, C, Le Quesne, J, John, T, Boutros, PC, Zhang, S-D, Fennell, DA, Busacca, S, Zhang, Q, Sharkey, A, Dawson, AG, Moore, DA, Waller, DA, Nakas, A, Jones, C, Cain, K, Luo, J-L, Salcedo, A, Salaroglio, IC, Riganti, C, Le Quesne, J, John, T, Boutros, PC, Zhang, S-D, and Fennell, DA

Abstract

We hypothesized that small molecule transcriptional perturbation could be harnessed to target a cellular dependency involving protein arginine methyltransferase 5 (PRMT5) in the context of methylthioadenosine phosphorylase (MTAP) deletion, seen frequently in malignant pleural mesothelioma (MPM). Here we show, that MTAP deletion is negatively prognostic in MPM. In vitro, the off-patent antibiotic Quinacrine efficiently suppressed PRMT5 transcription, causing chromatin remodelling with reduced global histone H4 symmetrical demethylation. Quinacrine phenocopied PRMT5 RNA interference and small molecule PRMT5 inhibition, reducing clonogenicity in an MTAP-dependent manner. This activity required a functional PRMT5 methyltransferase as MTAP negative cells were rescued by exogenous wild type PRMT5, but not a PRMT5E444Q methyltransferase-dead mutant. We identified c-jun as an essential PRMT5 transcription factor and a probable target for Quinacrine. Our results therefore suggest that small molecule-based transcriptional perturbation of PRMT5 can leverage a mutation-selective vulnerability, that is therapeutically tractable, and has relevance to 9p21 deleted cancers including MPM.

Published
2021

18. Sphingolipid synthesis inhibition by myriocin administration enhances lipid consumption and ameliorates lipid response to myocardial ischemia reperfusion injury

Author

Bonezzi F., Piccoli M., Cas M. D., Paroni R., Mingione A., Monasky M. M., Caretti A., Riganti C., Ghidoni R., Pappone C., Anastasia L., Signorelli P., Bonezzi, F., Piccoli, M., Cas, M. D., Paroni, R., Mingione, A., Monasky, M. M., Caretti, A., Riganti, C., Ghidoni, R., Pappone, C., Anastasia, L., and Signorelli, P.

Subjects
Ceramide, Sphingolipids, Metabolism, Physiology, Ischemia, Myriocin, Physiology (medical), Reperfusion, Original Research
Abstract

Myocardial infarct requires prompt thrombolytic therapy or primary percutaneous coronary intervention to limit the extent of necrosis, but reperfusion creates additional damage. Along with reperfusion, a maladaptive remodeling phase might occur and it is often associated with inflammation, oxidative stress, as well as a reduced ability to recover metabolism homeostasis. Infarcted individuals can exhibit reduced lipid turnover and their accumulation in cardiomyocytes, which is linked to a deregulation of peroxisome proliferator activated receptors (PPARs), controlling fatty acids metabolism, energy production, and the anti-inflammatory response. We previously demonstrated that Myriocin can be effectively used as post-conditioning therapeutic to limit ischemia/reperfusion-induced inflammation, oxidative stress, and infarct size, in a murine model. In this follow-up study, we demonstrate that Myriocin has a critical regulatory role in cardiac remodeling and energy production, by up-regulating the transcriptional factor EB, PPARs nuclear receptors and genes involved in fatty acids metabolism, such as VLDL receptor, Fatp1, CD36, Fabp3, Cpts, and mitochondrial FA dehydrogenases. The overall effects are represented by an increased β-oxidation, together with an improved electron transport chain and energy production. The potent immunomodulatory and metabolism regulatory effects of Myriocin elicit the molecule as a promising pharmacological tool for post-conditioning therapy of myocardial ischemia/reperfusion injury.

Published
2019

20. Consensus guidelines for the definition, detection and interpretation of immunogenic cell death

Author

Galluzzi, L., Vitale, I., Warren, S., Adjemian, S., Agostinis, P., Martinez, A.B., Chan, T.A., Coukos, G., Demaria, S., Deutsch, E., Draganov, D., Edelson, R.L., Formenti, S.C., Fucikova, J., Gabriele, L., Gaipl, U.S., Gameiro, S.R., Garg, A.D., Golden, E., Han, J., Harrington, K.J., Hemminki, A., Hodge, J.W., Hossain, DMS, Illidge, T., Karin, M., Kaufman, H.L., Kepp, O., Kroemer, G., Lasarte, J.J., Loi, S., Lotze, M.T., Manic, G., Merghoub, T., Melcher, A.A., Mossman, K.L., Prosper, F., Rekdal, Ø., Rescigno, M., Riganti, C., Sistigu, A., Smyth, M.J., Spisek, R., Stagg, J., Strauss, B.E., Tang, D., Tatsuno, K., van Gool, S.W., Vandenabeele, P., Yamazaki, T., Zamarin, D., Zitvogel, L., Cesano, A., Marincola, F.M., Department of Oncology, HUS Comprehensive Cancer Center, Research Programs Unit, TRIMM - Translational Immunology Research Program, University of Helsinki, and Helsinki University Hospital Area

Subjects
CALRETICULIN EXPOSURE, Consensus, Guidelines as Topic, Humans, Immunogenic Cell Death/genetics, Molecular Biology/methods, immunology, molecular biology, oncology, NOD-LIKE RECEPTORS, NF-KAPPA-B, 3122 Cancers, ANTICANCER CHEMOTHERAPY, IMMUNE CHECKPOINT BLOCKADE, ANTITUMOR IMMUNITY, ANTIGEN PRESENTATION, PATTERN-RECOGNITION RECEPTORS, APOPTOTIC CELLS, 3111 Biomedicine, CANCER-CELLS
Abstract

Cells succumbing to stress via regulated cell death (RCD) can initiate an adaptive immune response associated with immunological memory, provided they display sufficient antigenicity and adjuvanticity. Moreover, multiple intracellular and microenvironmental features determine the propensity of RCD to drive adaptive immunity. Here, we provide an updated operational definition of immunogenic cell death (ICD), discuss the key factors that dictate the ability of dying cells to drive an adaptive immune response, summarize experimental assays that are currently available for the assessment of ICD in vitro and in vivo, and formulate guidelines for their interpretation.

Published
2020

23. Mutant p53 induces SIRT3/MnSOD axis to moderate ROS production in melanoma cells

Author

Torrens-Mas M., Cordani M., Mullappilly N., Pacchiana R., Riganti C., Palmieri M., Pons D.G., Roca P., Oliver J., Donadelli M. and This work was supported by Italian Ministry of Education, University and Research (MIUR) , by the Comunidad de Madrid ( IND2017/IND-7809 ) and by grant from Fondo de Investigaciones Sanitarias of Instituto de Salud Carlos III ( PI14/01434 ) of the Spanish Government confinanced by FEDER-Unión Europea ('Una manera de hacer Europa'). Margalida Torrens-Mas was supported with a fellow by the Spanish Government ( FPU14/07042 ), by Consorzio Interuniversitario Biotecnologie (CIB) and by Federation of European Biochemical Societies (FEBS) .

Published
2020

24. Mutant p53-associated molecular mechanisms of ROS regulation in cancer cells

Author

Cordani M., Butera G., Pacchiana R., Masetto F., Mullappilly N., Riganti C., Donadelli M. and Funding: This work was partially supported by the Comunidad de Madrid (IND2017/IND-7809). IMDEA Nanociencia acknowledges support from the ‘Severo Ochoa’ Programme for Centres of Excellence in R&D (MINECO, Grant SEV-2016-0686).

Published
2020

25. HIF-1α is over-expressed in leukemic cells from TP53-disrupted patients and is a promising therapeutic target in chronic lymphocytic leukemia

Author

Griggio, V., Vitale, C., Todaro, M., Riganti, C., Kopecka, J., Salvetti, C., Bomben, R., M. D., Bo, Magliulo, D., Rossi, D., Pozzato, G., Bonello, L., Marchetti, M., Omede, P., Kodipad, A. A., Laurenti, L., Poeta, G. D., Mauro, F. R., Bernardi, R., Zenz, T., Gattei, V., Gaidano, G., Foa, R., Massaia, M., Boccadoro, M., and Coscia, M.

Subjects
Animals, Humans, Hypoxia-Inducible Factor 1, alpha Subunit, Mice, Phosphatidylinositol 3-Kinases, Tumor Microenvironment, Tumor Suppressor Protein p53, Von Hippel-Lindau Tumor Suppressor Protein, Leukemia, Lymphocytic, Chronic, B-Cell
Published
2020

27. Consensus guidelines for the definition, detection and interpretation of immunogenic cell death

Author

Galluzzi, L, Vitale, I, Warren, S, Adjemian, S, Agostinis, P, Buque Martinez, A, Chan, TA, Coukos, G, Demaria, S, Deutsch, E, Draganov, D, Edelson, RL, Formenti, SC, Fucikova, J, Gabriele, L, Gaipl, US, Gameiro, SR, Garg, AD, Golden, E, Han, J, Harrington, KJ, Hemminki, A, Hodge, JW, Hossain, DMS, Illidge, T, Karin, M, Kaufman, HL, Kepp, O, Kroemer, G, Lasarte, JJ, Loi, S, Lotze, MT, Manic, G, Merghoub, T, Melcher, AA, Mossman, KL, Prosper, F, Rekdal, O, Rescigno, M, Riganti, C, Sistigu, A, Smyth, MJ, Spisek, R, Stagg, J, Strauss, BE, Tang, D, Tatsuno, K, van Gool, SW, Vandenabeele, P, Yamazaki, T, Zamarin, D, Zitvogel, L, Cesano, A, Marincola, FM, Galluzzi, L, Vitale, I, Warren, S, Adjemian, S, Agostinis, P, Buque Martinez, A, Chan, TA, Coukos, G, Demaria, S, Deutsch, E, Draganov, D, Edelson, RL, Formenti, SC, Fucikova, J, Gabriele, L, Gaipl, US, Gameiro, SR, Garg, AD, Golden, E, Han, J, Harrington, KJ, Hemminki, A, Hodge, JW, Hossain, DMS, Illidge, T, Karin, M, Kaufman, HL, Kepp, O, Kroemer, G, Lasarte, JJ, Loi, S, Lotze, MT, Manic, G, Merghoub, T, Melcher, AA, Mossman, KL, Prosper, F, Rekdal, O, Rescigno, M, Riganti, C, Sistigu, A, Smyth, MJ, Spisek, R, Stagg, J, Strauss, BE, Tang, D, Tatsuno, K, van Gool, SW, Vandenabeele, P, Yamazaki, T, Zamarin, D, Zitvogel, L, Cesano, A, and Marincola, FM

Abstract

Cells succumbing to stress via regulated cell death (RCD) can initiate an adaptive immune response associated with immunological memory, provided they display sufficient antigenicity and adjuvanticity. Moreover, multiple intracellular and microenvironmental features determine the propensity of RCD to drive adaptive immunity. Here, we provide an updated operational definition of immunogenic cell death (ICD), discuss the key factors that dictate the ability of dying cells to drive an adaptive immune response, summarize experimental assays that are currently available for the assessment of ICD in vitro and in vivo, and formulate guidelines for their interpretation.

Published
2020

33. What sustains the multidrug resistance phenotype beyond ABC efflux transporters? Looking beyond the tip of the iceberg

Author

Alexa-Stratulat, T. Pešić, M. Gašparović, A.Č. Trougakos, I.P. Riganti, C.

Abstract

Identification of multidrug (MDR) efflux transporters that belong to the ATP-Binding Cassette (ABC) superfamily, represented an important breakthrough for understanding cancer multidrug resistance (MDR) and its possible overcoming. However, recent data indicate that drug resistant cells have a complex intracellular physiology that involves constant changes in energetic and oxidative-reductive metabolic pathways, as well as in the molecular circuitries connecting mitochondria, endoplasmic reticulum (ER) and lysosomes. The aim of this review is to discuss the key molecular mechanisms of cellular reprogramming that induce and maintain MDR, beyond the presence of MDR efflux transporters. We specifically highlight how cancer cells characterized by high metabolic plasticity – i.e. cells able to shift the energy metabolism between glycolysis and oxidative phosphorylation, to survive both the normoxic and hypoxic conditions, to modify the cytosolic and mitochondrial oxidative-reductive metabolism, are more prone to adapt to exogenous stressors such as anti-cancer drugs and acquire a MDR phenotype. Similarly, we discuss how changes in mitochondria dynamics and mitophagy rates, changes in proteome stability ensuring non-oncogenic proteostatic mechanisms, changes in ubiquitin/proteasome- and autophagy/lysosome-related pathways, promote the cellular survival under stress conditions, along with the acquisition or maintenance of MDR. After dissecting the complex intracellular crosstalk that takes place during the development of MDR, we suggest that mapping the specific adaptation pathways underlying cell survival in response to stress and targeting these pathways with potent pharmacologic agents may be a new approach to enhance therapeutic efficacy against MDR tumors. © 2019 Elsevier Ltd

Published
2019

38. GIFC-2018 - BOOK OF ABSTRACTS

Author

Muntoni, E, Battaglia, L, Marini, E, Giorgis, M, Lazzarato, L, Salaroglio, Ic, Riganti, C, and Martina, K

Published
2018

45. Comparison of Allogeneic and Syngeneic Rat Glioma Models by Using MRI and Histopathologic Evaluation

Author

Biasibetti, E., Valazza, A., Capucchio, M. T., Annovazzi, L., Battaglia, L., Chirio, D., Gallarate, M., Mellai, M., Elisabetta MUNTONI, Peira, E., Riganti, C., Schiffer, D., Panciani, P., and Lanotte, M.

Subjects
Rat Models, Isografts, Reproducibility of Results, Glioma, Allografts, Magnetic Resonance Imaging, Rats, Inbred F344, Rats, Disease Models, Animal, CNS, Brain Glioma Model, Animals, Rats, Wistar
Abstract

Research in neurooncology traditionally requires appropriate in vivo animal models, on which therapeutic strategies are tested before human trials are designed and proceed. Several reproducible animal experimental models, in which human physiologic conditions can be mimicked, are available for studying glioblastoma multiforme. In an ideal rat model, the tumor is of glial origin, grows in predictable and reproducible patterns, closely resembles human gliomas histopathologically, and is weakly or nonimmunogenic. In the current study, we used MRI and histopathologic evaluation to compare the most widely used allogeneic rat glioma model, C6-Wistar, with the F98-Fischer syngeneic rat glioma model in terms of percentage tumor growth or regression and growth rate. In vivo MRI demonstrated considerable variation in tumor volume and frequency between the 2 rat models despite the same stereotactic implantation technique. Faster and more reproducible glioma growth occurred in the immunoresponsive environment of the F98-Fischer model, because the immune response is minimized toward syngeneic cells. The marked inability of the C6-Wistar allogeneic system to generate a reproducible model and the episodes of spontaneous tumor regression with this system may have been due to the increased humoral and cellular immune responses after tumor implantation.

Published
2017

Catalog

Books, media, physical & digital resources
See catalog results