کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8303896 | 1537956 | 2013 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
TRPC3 regulates release of brain-derived neurotrophic factor from human airway smooth muscle
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کلمات کلیدی
bronchial alveolar lavageROISOCEGFPSTIM1NGFBALASM1,2-Bis(o-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid - 1،2-Bis (o-aminophenoxy) اتان N، N، N '، N'-tetraacetic اسیدBDNF - BDNF یا فاکتور نورونزایی مشتقشده از مغز siRNA - siRNAenzyme linked immunosorbent assay - آنزیم تست ایمونوسیورسانس مرتبط استBAPTA - بیایپیتیایELISA - تست الیزاAirway smooth muscle - عضله صاف راه هواییnerve growth factor - فاکتور رشد عصبBrain-derived neurotrophic factor - فاکتور نوروتروفی مشتق شده از مغزregion of interest - منطقه مورد نظرNeurotrophins - نوروتروفین Store-operated calcium entry - واردات کلسیم در فروشگاهgreen fluorescent protein - پروتئین فلورسنت سبز
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
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چکیده انگلیسی
Exogenous brain-derived neurotrophic factor (BDNF) enhances Ca2 + signaling and cell proliferation in human airway smooth muscle (ASM), especially with inflammation. Human ASM also expresses BDNF, raising the potential for autocrine/paracrine effects. The mechanisms by which ASM BDNF secretion occurs are not known. Transient receptor potential channels (TRPCs) regulate a variety of intracellular processes including store-operated Ca2 + entry (SOCE; including in ASM) and secretion of factors such as cytokines. In human ASM, we tested the hypothesis that TRPC3 regulates BDNF secretion. At baseline, intracellular BDNF was present, and BDNF secretion was detectable by enzyme linked immunosorbent assay (ELISA) of cell supernatants or by real-time fluorescence imaging of cells transfected with GFP-BDNF vector. Exposure to the pro-inflammatory cytokine tumor necrosis factor-alpha (TNFα) (20 ng/ml, 48 h) or a mixture of allergens (ovalbumin, house dust mite, Alternaria, and Aspergillus extracts) significantly enhanced BDNF secretion and increased TRPC3 expression. TRPC3 knockdown (siRNA or inhibitor Pyr3; 10 μM) blunted BDNF secretion, and prevented inflammation effects. Chelation of extracellular Ca2 + (EGTA; 1 mM) or intracellular Ca2 + (BAPTA; 5 μM) significantly reduced secreted BDNF, as did the knockdown of SOCE proteins STIM1 and Orai1 or plasma membrane caveolin-1. Functionally, secreted BDNF had autocrine effects suggested by phosphorylation of high-affinity tropomyosin-related kinase TrkB receptor, prevented by chelating extracellular BDNF with chimeric TrkB-Fc. These data emphasize the role of TRPC3 and Ca2 + influx in the regulation of BDNF secretion by human ASM and the enhancing effects of inflammation. Given the BDNF effects on Ca2 + and cell proliferation, BDNF secretion may contribute to altered airway structure and function in diseases such as asthma.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Cell Research - Volume 1833, Issue 12, December 2013, Pages 2953-2960
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Cell Research - Volume 1833, Issue 12, December 2013, Pages 2953-2960
نویسندگان
Pawan K. Vohra, Michael A. Thompson, Venkatachalem Sathish, Alexander Kiel, Calvin Jerde, Christina M. Pabelick, Brij B. Singh, Y.S. Prakash,