کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8303834 | 1537956 | 2013 | 13 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Ca2 + spiking activity caused by the activation of store-operated Ca2 + channels mediates TNF-α release from microglial cells under chronic purinergic stimulation
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کلمات کلیدی
yellow cameleonBSSBzATP2-APBPPADSDAPIMARCOUDPGAPDHEGTADMEMPBSbuffered salt solutionpyridoxal-phosphate-6-azophenyl-2′,4′-disulfonic acid4′,6-diamidino-2-phenylindole - 4 '، 6-دیامیدینو-2-فنیلینولDulbecco's modified Eagle Medium - Eagle Medium اصلاح شده DulbeccosiRNA - siRNAuridine diphosphate - uridine دی فسفاتOrai - آب و هواethylene glycol tetraacetic acid - اتیلن گلیکول تتراستیک اسیدCytokine release - انتشار سیتوکینanalysis of variance - تحلیل واریانسANOVA - تحلیل واریانس Analysis of variancetumor necrosis factor α - تومور نکروز عامل αcytomegalovirus - سیتومگالوویروسCMV - سیتومگالوویروسSOC - سیستم روی یک تراشهTNF-α - فاکتور نکروز توموری آلفاMacrophage - ماکروفاژ Phosphate-buffered saline - محلول نمک فسفات با خاصیت بافریMicroglia - میکروگلیاهاCalcium oscillation - نوسان کلسیمStore-operated channel - کانال ذخیره شدهglyceraldehyde 3-phosphate dehydrogenase - گلیسرولیدید 3-فسفات دهیدروژناز
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Ca2 + spiking activity caused by the activation of store-operated Ca2 + channels mediates TNF-α release from microglial cells under chronic purinergic stimulation Ca2 + spiking activity caused by the activation of store-operated Ca2 + channels mediates TNF-α release from microglial cells under chronic purinergic stimulation](/preview/png/8303834.png)
چکیده انگلیسی
Cytokines released from microglia mediate defensive responses in the brain, but the underlying mechanisms are obscure. One proposed process is that nucleotide leakage or release from surrounding cells is sensed by metabotropic (P2Y) and ionotropic (P2X) purinergic receptors, which may trigger long-term intracellular Ca2 + flux and tumor necrosis factor α (TNF-α) release. Indeed, 3 h of exposure to ATP was required to evoke TNF-α release from a murine microglial cell line (MG5). A Ca2 + chelator, ethylene glycol tetraacetic acid (EGTA), reduced ATP-induced TNF-α release, suggesting that intracellular Ca2 + is important in this response. Therefore, Ca2 + sensor genes (YC3.6) were transfected into MG5 cells to investigate the Ca2 + dynamics underlying ATP-induced TNF-α release. The results demonstrated ATP-induced biphasic Ca2 + mobilization mediated by P2Y (~ 5 min) and P2X7 receptors (5-30 min). Moreover, Ca2 + spiking activity in cell processes progressively increased with a reduction in P2X7 receptor-mediated Ca2 + elevation during 3-h ATP stimulation. Increased Ca2 + spiking activity paralleled the reduction in thapsigargin-sensitive internal Ca2 + stores, dendrite extension, and expression of macrophage scavenger receptors with collagenous structure. The Ca2 + spiking activity was enhanced by a P2X7 receptor antagonist (A438079), but inhibited by a store-operated channel antagonist (SKF96365) or by co-transfection of small interference ribonucleic acid (siRNA) targeted on the channel component (Orai1). Furthermore, ATP-induced TNF-α release was enhanced by A438079 but was inhibited by SKF96365. Because store-operated channels (Stim1/Orai1) were expressed both in MG5 and primary microglial cultures, we suggest that P2X7 receptor signaling inhibits store-operated channels during ATP stimulation, and disinhibition of this process gates TNF-α release from microglial cells.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Cell Research - Volume 1833, Issue 12, December 2013, Pages 2573-2585
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Cell Research - Volume 1833, Issue 12, December 2013, Pages 2573-2585
نویسندگان
Masayuki Ikeda, Saki Tsuno, Takashi Sugiyama, Ayami Hashimoto, Kurumi Yamoto, Kouhei Takeuchi, Hiroyuki Kishi, Hiroyuki Mizuguchi, Shin-ichi Kohsaka, Tohru Yoshioka,