26 results on '"Xuexin Zhang"'
Search Results
2. STIM1 is a core trigger of airway smooth muscle remodeling and hyperresponsiveness in asthma.
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Johnson, Martin T., Ping Xin, Benson, J. Cory, Pathak, Trayambak, Walter, Vonn, Emrich, Scott M., Yoast, Ryan E., Xuexin Zhang, Gaoyuan Cao, Panettieri Jr., Reynold A., and Trebak, Mohamed
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SMOOTH muscle ,AIRWAY (Anatomy) ,ASTHMA ,EXTRACELLULAR matrix ,GROWTH factors ,REMANUFACTURING ,COMMERCIAL products - Abstract
Airway remodeling and airway hyperresponsiveness are central drivers of asthma severity. Airway remodeling is a structural change involving the dedifferentiation of airway smooth muscle (ASM) cells from a quiescent to a proliferative and secretory phenotype. Here, we show up-regulation of the endoplasmic reticulum Ca
2+ sensor stromal-interacting molecule 1 (STIM1) in ASM of asthmatic mice. STIM1 is required for metabolic and transcriptional reprogramming that supports airway remodeling, including ASM proliferation, migration, secretion of cytokines and extracellular matrix, enhanced mitochondrial mass, and increased oxidative phosphorylation and glycolytic flux. Mechanistically, STIM1- mediated Ca2+ influx is critical for the activation of nuclear factor of activated T cells 4 and subsequent interleukin-6 secretion and transcription of pro-remodeling transcription factors, growth factors, surface receptors, and asthma-associated proteins. STIM1 drives airway hyperresponsiveness in asthmatic mice through enhanced frequency and amplitude of ASM cytosolic Ca2+ oscillations. Our data advocates for ASM STIM1 as a target for asthma therapy. [ABSTRACT FROM AUTHOR]- Published
- 2022
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3. PKC-ε regulates vesicle delivery and focal exocytosis for efficient IgG-mediated phagocytosis.
- Author
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D'Amico, Anna E., Wong, Alexander C., Zajd, Cheryl M., Xuexin Zhang, Murali, Ananya, Trebak, Mohamed, and Lennartz, Michelle R.
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EXOCYTOSIS ,PROTEIN kinase C ,CATALYTIC activity ,PHAGOSOMES ,MICROTUBULES - Abstract
Protein kinase C (PKC)-ε is required for membrane addition during IgG-mediated phagocytosis, but its role in this process is ill defined. Here, we performed high-resolution imaging, which reveals that PKC- ε exits the Golgi and enters phagosomes on vesicles that then fuse. TNF and PKC-ε colocalize at the Golgi and on vesicles that enter the phagosome. Loss of PKC-ε and TNF delivery upon nocodazole treatment confirmed vesicular transport on microtubules. That TNF+ vesicles were not delivered in macrophages from PKC-ε null mice, or upon dissociation of the Golgi-associated pool of PKC-ε, implies that Golgi-tethered PKC-ε is a driver of Golgi-to-phagosome trafficking. Finally, we established that the regulatory domain of PKC-ε is sufficient for delivery of TNF+ vesicles to the phagosome. These studies reveal a novel role for PKC-ε in focal exocytosis -- its regulatory domain drives Golgi-derived vesicles to the phagosome, whereas catalytic activity is required for their fusion. This is one of the first examples of a PKC requirement for vesicular trafficking and describes a novel function for a PKC regulatory domain. This article has an associated First Person interview with the first author of the paper. [ABSTRACT FROM AUTHOR]
- Published
- 2021
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4. Dichotomous role of the human mitochondrial Na+/Ca2+/Li+ exchanger NCLX in colorectal cancer growth and metastasis.
- Author
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Pathak, Trayambak, Gueguinou, Maxime, Walter, Vonn, Delierneux, Celine, Johnson, Martin T., Xuexin Zhang, Ping Xin, Yoast, Ryan E., Emrich, Scott M., Yochum, Gregory S., Sekler, Israel, Koltun, Walter A., Gill, Donald L., Hempel, Nadine, and Trebak, Mohamed
- Published
- 2020
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5. L-type Ca2+ channel blockers promote vascular remodeling through activation of STIM proteins.
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Johnson, Martin T., Gudlur, Aparna, Xuexin Zhang, Ping Xin, Emrich, Scott M., Yoast, Ryan E., Courjaret, Raphael, Nwokonko, Robert M., Wei Li, Hempel, Nadine, Machaca, Khaled, Gill, Donald L., Hogan, Patrick G., and Trebak, Mohamed
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VASCULAR remodeling ,VASCULAR smooth muscle ,OLDER patients ,BLOOD proteins ,ENDOPLASMIC reticulum - Abstract
Voltage-gated L-type Ca2+ channel (Cav1.2) blockers (LCCBs) are major drugs for treating hypertension, the preeminent risk factor for heart failure. Vascular smooth muscle cell (VSMC) remodeling is a pathological hallmark of chronic hypertension. VSMC remodeling is characterized by molecular rewiring of the cellular Ca2+ signaling machinery, including down-regulation of Cav1.2 channels and up-regulation of the endoplasmic reticulum (ER) stromalinteracting molecule (STIM) Ca2+ sensor proteins and the plasma membrane ORAI Ca2+ channels. STIM/ORAI proteins mediate storeoperated Ca2+ entry (SOCE) and drive fibro-proliferative gene programs during cardiovascular remodeling. SOCE is activated by agonists that induce depletion of ER Ca2+, causing STIM to activate ORAI. Here, we show that the three major classes of LCCBs activate STIM/ORAI-mediated Ca2+ entry in VSMCs. LCCBs act on the STIM N terminus to cause STIM relocalization to junctions and subsequent ORAI activation in a Cav1.2-independent and store depletionindependent manner. LCCB-induced promotion of VSMC remodeling requires STIM1, which is up-regulated in VSMCs from hypertensive rats. Epidemiology showed that LCCBs are more associated with heart failure than other antihypertensive drugs in patients. Our findings unravel a mechanism of LCCBs action on Ca2+ signaling and demonstrate that LCCBs promote vascular remodeling through STIM-mediated activation of ORAI. Our data indicate caution against the use of LCCBs in elderly patients or patients with advanced hypertension and/or onset of cardiovascular remodeling, where levels of STIM and ORAI are elevated. [ABSTRACT FROM AUTHOR]
- Published
- 2020
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6. IMI's Teaching Design, Feedback System and its Localization.
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Tingting Wen and Xuexin Zhang
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- 2017
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7. The PAD Class, a new paradigm for university classroom teaching.
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Xuexin Zhang
- Published
- 2017
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8. Extremal Matching Energy of Random Polyomino Chains.
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Tingzeng Wu, Huazhong Lü, and Xuexin Zhang
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LAPLACIAN matrices ,GRAPH theory ,LAPLACIAN operator ,HERMITIAN operators ,POLYOMINOES - Abstract
Polyomino graphs is one of the research objectives in statistical physics and in modeling problems of surface chemistry. A random polyomino chain is a subgraph of a polyomino graph. The matching energy is defined as the sum of the absolute values of the zeros of the matching polynomial of a graph. In this paper, we characterize the graphs with the extremal matching energy among all random polyomino chains of a polyomino graph by the probability method. [ABSTRACT FROM AUTHOR]
- Published
- 2017
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9. Expression and prognostic value of SFRP1 and β-catenin in patients with glioblastoma.
- Author
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LIANG CHANG, XUHUI LEI, YU QIN, GUANGCHUN ZENG, XUEXIN ZHANG, HUA JIN, CHAO WANG, XIN WANG, and JUN SU
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PROTEIN expression ,CATENINS ,GLIOBLASTOMA multiforme ,IMMUNOHISTOCHEMISTRY ,ADJUVANT treatment of cancer ,KAPLAN-Meier estimator - Abstract
The roles of secreted frizzled-related protein-1 (SFRP1) and β-catenin in human cancer have been widely studied, and it has recently been demonstrated that these proteins are associated with numerous human carcinomas. However, their clinical significance in glioblastoma multi-forme (GBM) has not been examined. The current study aimed to analyze the correlation between the expression of SFRP1 and β-catenin, and clinicopathological characteristics in GBM patients. The expression of SFRP1 and β-catenin was assessed by immunohistochemistry in 113 samples of GBM and 40 normal brain tissues. Compared with normal brain tissues, GBM tissues exhibited significantly lower expression of SFRP1, and higher expression of β-catenin (both P<0.05). A Kaplan-Meier analysis revealed that patients with positive SFRP1 expression had a significantly longer overall survival (OS) time relative to those with negative SFRP1 expression (P<0.000), and that patients with positive β-catenin expression had a shorter OS time than those with negative β-catenin expression (P<0.000). A multivariate Cox regression analysis indicated that adjuvant treatment, SFRP1 expression and β-catenin expression were independent prognostic factors for OS (P<0.000, P=0.008 and P=0.001, respectively) in patients with GBM. The current data suggest that expression of SFRP1 and β-catenin may be considered significant prognostic indicators for patients with GBM. [ABSTRACT FROM AUTHOR]
- Published
- 2016
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10. MicroRNA-133b inhibits cell migration and invasion by targeting matrix metalloproteinase 14 in glioblastoma.
- Author
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LIANG CHANG, XUHUI LEI, YU QIN, XUEXIN ZHANG, HUA JIN, CHAO WANG, XIN WANG, GUOFU LI, CHUNLEI TAN, and JUN SU
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GLIOBLASTOMA multiforme ,MICRORNA ,CELL migration ,MATRIX metalloproteinases ,ENDOPEPTIDASES - Abstract
Increasing evidence has suggested that microRNA-133b (miR-133b) is important in regulating the genesis of different types of cancer. However, the effects and the underlying mechanisms of miR-133b in the development of glioblastoma (GBM) remain largely unknown. The aim of the present study was to investigate the role of miR-133b in GBM and to determine the molecular mechanisms underlying its action. Reverse transcription-quantitative polymerase chain reaction was used to measure the expression levels of miR-133b in 21 human GBM samples and 9 normal brain tissue samples. A wound healing assay, and Transwell migration and invasion assays were used to evaluate the effects of miR-133b on cell migration and invasion. Western blotting and a luciferase reporter assay were used to identify the target genes of miR-133b. It was found that miR-133b suppressed GBM cell migration and invasion, and matrix metalloproteinase 14 (MMP14) was identified as a direct target gene. In conclusion, miR-133b may suppress GBM migration and invasion through directly targeting MMP14, highlighting its potential as a novel agent for the treatment of GBM invasion. [ABSTRACT FROM AUTHOR]
- Published
- 2015
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11. RNA interference-mediated knockdown of translationally controlled tumor protein induces apoptosis, and inhibits growth and invasion in glioma cells.
- Author
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HUA JIN, XUEXIN ZHANG, JUN SU, YUEQIU TENG, HUAN REN, and LIZHUANG YANG
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RNA interference ,TUMOR proteins ,APOPTOSIS ,GLIOMAS ,GENE expression - Abstract
Translationally controlled tumor protein (TCTP) is a highly conserved, growth-associated and small molecule protein, which is highly expressed in various types of tumor cell. TCTP can promote the growth and suppress apoptosis of tumor cels. However, few studies have reported the effects of TCTP in gliomas. In the present study, a glioma cell line was established, which was stably transfected with TCTP short hairpin ribonucleic acid (shRNA), to investigate the impact of downregulated expression of TCTP on the proliferation, apoptosis and invasion of glioma cells. Western blot and reverse transcription-quantitative polymerase chain reaction analyses demonstrated that TCTP shRNA effectively reduced the expression of TCTP in the U251 glioma cell line. MTT and colony formation assays revealed that downregulated expression of TCTP significantly inhibited glioma cell proliferation. Cell cycle analysis using flow cytometry revealed that the cells in the pRNA-H1.1-TCTP group were arrested in the G0/G1 phase of the cell cycle. Western blot analysis detected downregulated expression levels of cyclins, including Cyclin D1, Cyclin E and Cyclin B. Annexin V-fluorescein isothiocyanate/ propidium iodide and Hoechst staining demonstrated that the apoptotic rate of the cells in the pRNA-H1.1-TCTP group was significantly higher than that of the cells in the pRNA-H1.1-control group, with upregulated expression levels of B-cell-associated X protein and cleaved-caspase-3 and downregulated expression of B-cell lmyphoma-2 in the apoptotic process. Wound healing and Transwell assays revealed that downregulated expression of TCTP significantly inhibited the migration and invasiveness of the glioma cells; and the expression levels and activities of matrix metalloproteinase (MMP)-2 and MMP-9 were also significantly affected. In conclusion, the present study demonstrated that downregulated expression of TCTP significantly inhibited proliferation and invasion, and induced apoptosis in the glioma cells. These results suggested that TCTP may be important in glioma development and metastasis. Therefore, TCTP is expected to become an effective target for glioma gene therapy. [ABSTRACT FROM AUTHOR]
- Published
- 2015
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12. Multiple types of calcium channels arising from alternative translation initiation of the Orai1 message.
- Author
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Desai, Pooja N., Xuexin Zhang, Shilan Wu, Janoshazi, Agnes, Bolimuntha, Sunitha, Putney, James W., and Trebak, Mohamed
- Published
- 2015
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13. BILINGUAL MEMORY REPRESENTATIONS IN LESS FLUENT CHINESE-ENGLISH BILINGUALS: AN EVENT-RELATED POTENTIAL STUDY.
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CHAO-YING CHEN, XUEXIN ZHANG, JOHN, LI LI, and RUIMING WANG
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BILINGUALISM ,LANGUAGE & languages ,CHINESE language ,ENGLISH language ,MEMORY - Abstract
The present study was designed to investigate bilingual memory representations in less fluent Chinese-English bilinguals and the effect of word familiarity on bilingual memory representations with a translation priming paradigm and the event-related potential (ERP) technique. Three factors (translation order, word familiarity, and repetition status) were manipulated in this study, and the major dependent variable was the magnitude of the N400 repetition effect, which is related to semantic expectation and is an important physiological index of language processing. The results confirmed the asymmetry in bilingual memory with stronger L2-LI links compared to L1-L2 links in less fluent Chinese-English bilinguals, and that word familiarity was an important factor in the memory representations of these less fluent bilinguals. [ABSTRACT FROM AUTHOR]
- Published
- 2015
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14. Synthesis of N-Benzothiazol-2-yl-amides by an Iron-Catalyzed Oxidative C(sp2)-H Functionalization.
- Author
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Junke Wang, Yingxiao Zong, Xuexin Zhang, Yang Gao, Zhengliang Li, Guoren Yue, Zhengjun Quan, and Xicun Wang
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ORGANIC synthesis ,ORGANIC compounds ,AMIDES ,IRON ores ,NATIVE element minerals - Abstract
Catalytic synthesis of N-benzothiazol-2-yl-amides from 1-acyl-3-(phenyl)thioureas was achieved in the presence of an iron catalyst through C(sp
2 )-H functionalization and C-S bond formation. Various N-benzothiazol-2-yl-amides were selectively obtained in good yields. [ABSTRACT FROM AUTHOR]- Published
- 2014
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15. The prosurvival role of autophagy inresveratrol-induced cytotoxicity in GH3 cells.
- Author
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XUEXIN ZHANG, WANHAI XU, JUN SU, MING CHU, HUA JIN, GUOFU LI, CHUNLEI TAN, XIN WANG, and CHAO WANG
- Published
- 2014
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16. Recombinant AAV-PR39-mediated hypoxia-inducible factor 1α gene expression attenuates myocardial infarction.
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LIJUN SUN, YUEWEN HAO, XIAOWEI NIE, JIAN XU, ZHENWU LI, WEI ZHANG, YING LIU, and XUEXIN ZHANG
- Published
- 2014
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17. Mechanisms of STIM1 Activation of Store-Independent Leukotriene C4-Regulated Ca2+ Channels.
- Author
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Xuexin Zhang, González-Cobos, José C., Schindl, Rainer, Muik, Martin, Ruhle, Brian, Motiani, Rajender K., Bisaillon, Jonathan M., Wei Zhang, Fahrner, Marc, Barroso, Margarida, Matrougui, Khalid, Romanin, Christoph, and Trebak, Mohamed
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MUSCLE cells ,MUSCLE cell culture ,GROWTH factors ,LEUKOTRIENES ,THROMBIN - Abstract
We recently showed, in primary vascular smooth muscle cells (VSMCs), that the platelet-derived growth factor activates canonical store-operated Ca
2+ entry and Ca2+ release-activated Ca2+ currents encoded by Orai1 and STIM1 genes. However, thrombin activates store-independent Ca2+ selective channels contributed by both Orai3 and Orai1. These store-independent Orai3/Orai1 channels are gated by cytosolic leukotriene C4 (LTC4) and require STIM1 downstream LTC4 action. However, the source of LTC4 and the signaling mechanisms of STIM1 in the activation of this LTC4 -regulated Ca2+ (LRC) channel are unknown. Here, we show that upon thrombin stimulation, LTC4 is produced through the sequential activities of phospholipase C, diacylglycerol lipase, 5-lipo-oxygenease, and leukotriene C4 synthase. We show that the endoplasmic reticulum-resident STIM1 is necessary and sufficient for LRC channel activation by thrombin. STIM1 does not form sustained puncta and does not colocalize with Orai1 either under basal conditions or in response to thrombin. However, STIM1 is precoupled to Orai3 and Orai3/Orai1 channels under basal conditions as shown using Forster resonance energy transfer (FRET) imaging. The second coiled-coil domain of STIM1 is required for coupling to either Orai3 or Orai3/Orai1 channels and for LRC channel activation. We conclude that STIM1 employs distinct mechanisms in the activation of store-dependent and store-independent Ca2+ entry pathways. [ABSTRACT FROM AUTHOR]- Published
- 2013
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18. STIM1 Controls Endothelial Barrier Function Independently of Orai1 and Ca2+ Entry.
- Author
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Shinde, Arti V., Motiani, Rajender K., Xuexin Zhang, Abdullaev, Iskandar F., Adam, Alejandro P., González-Cobos, José C., Wei Zhang, Matrougui, Khalid, Vincent, Peter A., and Trebak, Mohamed
- Published
- 2013
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19. Orai3 is an estrogen receptor α-regulated Ca2+ channel that promotes tumorigenesis.
- Author
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Motiani, Rajender K., Xuexin Zhang, Harmon, Kelly E., Keller, Rebecca S., Matrougui, Khalid, Bennett, James A., and Trebak, Mohamed
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ESTROGEN receptors ,CALCIUM channels ,CARCINOGENESIS ,BREAST cancer research ,CELL proliferation - Abstract
Store-operated Ca
2+ entry (SOCE) encoded by Orail proteins is a ubiquitous Ca2+ -selective conductance involved in cellular proliferation and mi- gration. We recently described up-regulation of Orai3 channels that selectively mediate SOCE in estrogen receptor α-expressing (ERα+ ) breast cancer cells. How- ever, the connection between ERα and Orai3 and the role of Orai3 in tumorigenesis remain unknown. Here, we show that ERot knockdown decreases Orai3 mRNA (by ~63%) and protein (by ~44%) with no effect on Orail. ERα knockdown decreases Orai3-mediated SOCE (by ~43%) and the corresponding Ca2+ release- activated Ca2+ (CRAC) current (by ~42%) in ERα+ MCF7 cells. The abrogation of SOCE in MCF7 cells on ERα knockdown can be rescued by ectopic expression of Orai3. ERα activation increased Orai3 expression and SOCE in MCF7 cells. Epidermal growth factor (EGF) and thrombin stimulate Ca2+ influx into MCF7 cells through Oral3. Orai3 knockdown inhibited SOCE- dependent phosphorylation of extracellular signal-regulated kinase (ERK1/2; by ~44%) and focal adhesion kinase (FAK; by ~46%) as well as transcriptional activity of nuclear factor for activated T cells (NFAT; by ~49%). Significantly, Orai3 knockdown selectively decreased anchorage-independent growth (by ~58%) and Matrigel invasion (by ~44%) of ERα+ MCF7 cells with no effect on ERα- MDA-MB231 cells. Moreover, Orai3 knockdown inhibited ERα+ cell tumorigenesis in immunodeficient mice (~66% reduction in tumor volume). These data establish Orai3 as an ERα-regulated channel and a potential selective therapeutic target for ERα+ breast cancers. [ABSTRACT FROM AUTHOR]- Published
- 2013
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20. Ryanodine Receptor Blockade Reduces Amyloid-ß Load and Memory Impairments in Tg2576 Mouse Model of Alzheimer Disease.
- Author
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Oulès, Bénédicte, Prête, Dolores Del, Greco, Barbara, Xuexin Zhang, Lauritzen, Inger, Sevalle, Jean, Moreno, Sebastien, Paterlini-Bréchot, Patrizia, Trebak, Mohamed, Checler, Frédéric, Benfenati, Fabio, and Chami, Mounia
- Subjects
ALZHEIMER'S disease ,PERTURBATION theory ,ENDOPLASMIC reticulum ,HOMEOSTASIS ,CALCIUM ,AMYLOID beta-protein precursor - Abstract
In Alzheimer disease (AD), the perturbation of the endoplasmic reticulum (ER) calcium (Ca
2+ ) homeostasis has been linked to prese-nilins, the catalytic core in γ-secretase complexes cleaving the amyloid precursor protein (APP), thereby generating amyloid-β (Aβ) peptides. Here we investigate whether APP contributes to ER Ca2+ homeostasis and whether ER Ca2+ could in turn influence Aβ production. We show that overexpression of wild-type human APP ( APP695 ), or APP harboring the Swedish double mutation (APPswe ) triggers increased ryanodine receptor (RyR) expression and enhances RyR-mediated ER Ca2+ release in SH-SY5Y neuroblastoma cells and in APPswe-expressing (Tg2576) mice. Interestingly, dantrolene-induced lowering of RyR-mediated Ca2+ release leads to the reduction of both intracellular and extracellular Aβ load in neuroblastoma cells as well as in primary cultured neurons derived from Tg2576 mice. This Aβ reduction can be accounted for by decreased Thr-668-dependent APP phosphorylation and β- and γ-secretases activities. Importantly, dantrolene diminishes Aβ load, reduces Aβ-related histological lesions, and slows down learning and memory deficits in Tg2576 mice. Overall, our data document a key role of RyR in Aβ production and learning and memory performances, and delineate RyR-mediated control of Ca2+ homeostasis as a physiological paradigm that could be targeted for innovative therapeutic approaches. [ABSTRACT FROM AUTHOR]- Published
- 2012
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21. NON-TARGET LANGUAGE PROCESSING IN CHINESE-ENGLISH BILINGUALS: A STUDY Of EVENT-RELATED POTENTIAL.
- Author
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LI LI, MENG FAN, BING SUN, RUIMING WANG, LEI MO, and XUEXIN ZHANG, JOHN
- Subjects
COGNITIVE processing of language ,EVOKED potentials (Electrophysiology) ,BILINGUALISM ,CHINESE language ,ENGLISH language ,PSYCHOLOGY - Abstract
The event-related brain potential (ERP) technique was used to investigate the neural mechanism of non-target language processing in Chinese-English bilinguals. Participants were presented with a mixed list of Chinese and English words and required to make conceptual decisions for words in one language and ignore words in the other non-target language. Regardless of whether the non-target word was in Chinese or English, the ERPs they elicited were modulated by word frequency, suggesting that their meaning had been accessed. The N400 peak was delayed in the English as the non-target language condition, probably because participants were less proficient in English. The results suggest that the non-target language can be processed during conceptual tasks with participants' proficiency in this language being a critical factor. [ABSTRACT FROM AUTHOR]
- Published
- 2012
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22. Enhanced Ca2+ entry due to Orail plasma membrane insertion increases IL-8 secretion by cystic fibrosis airways.
- Author
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Balghi, Haouaria, Robert, Renaud, Rappaz, Benjamin, Xuexin Zhang, Wohlhuter-Haddad, Adeline, Evagelidis, Alexandra, Luo, Yishan, Goepp, Julie, Ferraro, Pasquale, Romto, Philippe, Trebak, Mohamed, Wiseman, Paul W., Thomas, David Y., and Hanrahan, John W.
- Subjects
CYSTIC fibrosis ,LUNG diseases ,GENETIC disorders ,ENDOPLASMIC reticulum ,ORGANELLES - Abstract
Cystic fibrosis (CF) is caused by mutations in the gene encoding the CF transmembrane conductance regulator (CFTR). The most common mutation, AF508, causes retention of CFFR in the endoplasmic reticulum (ER). Some CF abnormalities can be explained by altered Ca
2+ homeostasis, although it remains unknown how CFTR influences calcium signaling. This study examined the novel hypothesis that store-operated calcium entry (SOCE) through Orail is abnormal in CF. The significance of Orail-mediated SOCE for increased interleukin-8 (IL-8) expression in CF was also investigated. CF and non-CF human airway epithelial cell line and primary cells (obtained at lung transplantation) were used in Ca2+ imaging, electrophysiology, and fluorescence imaging experiments to explore differences in Orail function in CF vs. non-CF cells. Protein expression and localization was assessed by Western blots, cell surface biotinylation, ELISA, and image correlation spectroscopy (ICS). We show here that store-operated Ca2+ entry (SOCE) is elevated in CF human airway epithelial cells (hAECs; ~1.8- and ~2.5-fold for total Ca2+ i increase and Ca2+ influx rate, respectively, and ~2-fold increase in the ICRAC current) and is caused by increased exocytotic insertion (~2-fold) of Orail channels into the plasma membrane, which is normalized by rescue of ΔF508-CFTR trafficking to the cell surface. Augmented SOCE in CF cells is a major factor leading to increased IL-8 secretion (~2-fold). CFTR normally down-regulates the Orail/stromal interaction molecule 1 (STIM1) complex, and loss of this inhibition due to the absence of CFTR at the plasma membrane helps to explain the potentiated inflammatory response in CF cells. [ABSTRACT FROM AUTHOR]- Published
- 2011
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23. PHONOLOGY AND ACCESS TO CHINESE CHARACTER MEANING1'2.
- Author
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LINGYUE KONG, JOHN XUEXIN ZHANG, CONNIE SUK-HAN HO, and CUIPING KANG
- Subjects
PHONOLOGY ,READING ,CHINESE characters ,SEMANTICS ,CHINESE language - Abstract
One of the central concerns in theories of reading skills is the role of phonology in access to word meaning. The present study focused on this issue in Chinese to examine the extent to which phonology affects Chinese character recognition. Two naming experiments were conducted with a phonologically mediated semantic priming paradigm, and the relative frequencies of semantic associates of the targets and their homophones were manipulated systematically. Analyses showed that a semantic associate produced robust priming on target naming at 57- and 250-msec. stimulus onset asynchronies, but only the low frequency homo- phones of high frequency semantic associates facilitated target naming at a 250- msec. stimulus onset asynchrony. These results indicate the role of phonology is neither obligatory nor efficient in access to Chinese character meaning, contradicting the key assumptions of the lexical constituency model. A revised parallel access model that emphasizes visual access to semantics is suggested as a more plausible account. [ABSTRACT FROM AUTHOR]
- Published
- 2010
- Full Text
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24. TWIK-1 and TREK-1 Are Potassium Channels Contributing Significantly to Astrocyte Passive Conductance in Rat Hippocampal Slices.
- Author
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Min Zhou, Guangjin Xu, Minjie Xie, Xuexin Zhang, Schools, Gary P., Liqun Ma, Kimelberg, Harold K., and Haijun Chen
- Subjects
POTASSIUM channels ,ION channels ,NEUROGLIA ,HIPPOCAMPUS (Brain) ,LABORATORY rats - Abstract
Expression of a linear current-voltage (I-V) relationship (passive) K
+ membrane conductance is a hallmark of mature hippocampal astrocytes. However, the molecular identifications of the K+ channels underlying this passive conductance remain unknown. We provide the following evidence supporting significant contribution of the two-pore domain K+ channel (K2P ) isoforms, TWIK-1 and TREK-1, to this conductance. First, both passive astrocytes and the cloned rat TWIK-1 and TREK-1 channels expressed in CHO cells conduct significant amounts of Cs+ currents, but vary in their relative PCs /PK permeability, 0.43, 0.10, and 0.05, respectively. Second, quinine, which potently inhibited TWIK-1 (IC50 = 85 μM) and TREK-1 (IC50 = 41 μM) currents, also inhibited astrocytic passive conductance by 58% at a concentration of 200 μM. Third, a moderate sensitivity of passive conductance to low extracellular pH (6.0) supports a combined expression of acid-insensitive TREK-1, and to a lesser extent, acid-sensitive TWIK-1. Fourth, the astrocyte passive conductance showed low sensitivity to extracellular Ba2+ , and extracellular Ba2+ blocked TWIK-1 channels at an IC50 of 960 μM and had no effect on TREK-1 channels. Finally, an immunocytochemical study showed colocalization of TWIK-1 and TREK-1 proteins with the astrocytic markers GLAST and GFAP in rat hippocampal stratum radiatum. In contrast, another K2P isoform TASK-1 was mainly colocalized with the neuronal marker NeuN in hippocampal pyramidal neurons and was expressed at a much lower level in astrocytes. These results support TWIK-1 and TREK-1 as being the major components of the long-sought K+ channels underlying the passive conductance of mature hippocampal astrocytes. [ABSTRACT FROM AUTHOR]- Published
- 2009
- Full Text
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25. The research of effect of various parameters on processing performance of compound machining of EDM milling and arc machining.
- Author
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Zhenwei Niu, Yonghong Liu, Xinlei Wu, Xuexin Zhang, and Zhiwei Ding
- Published
- 2019
- Full Text
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26. Leaky Ryanodine receptors increases Amyloidbeta load and induces memory impairments in Tg2576 mouse model of Alzheimer disease.
- Author
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Oulès, Bénédicte, Del Prete, Dolores, Greco, Barbara, Xuexin Zhang, Lauritzen, Inger, Trebak, Mohamed, Benfenati, Fabio, Checler, Frédéric, and Chami, Mounia
- Subjects
RYANODINE receptors ,ALZHEIMER'S disease - Abstract
An abstract of the article "Leaky Ryanodine receptors increases Amyloidbeta load and induces memory impairments in Tg2576 mouse model of Alzheimer disease" by Bénédicte Oulès and colleagues is presented.
- Published
- 2013
- Full Text
- View/download PDF
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