کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8259866 | 1534647 | 2015 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Calpain-1 induces endoplasmic reticulum stress in promoting cardiomyocyte apoptosis following hypoxia/reoxygenation
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کلمات کلیدی
ATF4hypoxia/re-oxygenationinositol-requiring kinase 1sarco/endoplasmic reticulum Ca2 +-ATPaseprotein kinase-like ER kinasetauroursodeoxycholateATF6eIF2αXBP1IRE1H/R - H / RI/R - I / RJNK1/2 - JNK1 / 2MOI - MEMyocardial infarction - آنفارکتوس میوکاردER stress - استرس استischemia/reperfusion - ایسکمی / رپرفیوژنCHOP - تکه کردنApoptosis - خزان یاختهایendoplasmic reticulum - شبکه آندوپلاسمی eukaryotic translation initiation factor 2α - عامل آغازگر ترجمه یوکاریوتی 2αactivating transcription factor 6 - فعال کردن عامل رونویسی 6CAST - قالبSERCA - قلبhypoxia/reoxygenation - هیپوکسیا / اکسیداسیون مجددX-box binding protein 1 - پروتئین اتصال X جعبه 1PERK - پرکmultiplicity of infection - چندین عفونتCalpain - کالپینCalpastatin - کپسالاتین
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Both calpain activation and endoplasmic reticulum (ER) stress are implicated in ischemic heart injury. However, the role of calpain in ER stress remains largely elusive. This study investigated whether calpain activation causes ER stress, thereby mediating cardiomyocyte apoptosis in an in vitro model of hypoxia/re-oxygenation (H/R). In neonatal mouse cardiomyocytes and rat cardiomyocyte-like H9c2 cells, up-regulation of calpain-1 sufficiently induced ER stress, c-Jun N-terminal protein kinase1/2 (JNK1/2) activation and apoptosis. Inhibition of ER stress or JNK1/2 prevented apoptosis induced by calpain-1. In an in vitro model of H/R-induced injury in cardiomyocytes, H/R was induced by a 24-hour hypoxia followed by a 24-hour re-oxygenation. H/R activated calpain-1, induced ER stress and JNK1/2 activation, and triggered apoptosis. Inhibition of calpain and ER stress blocked JNK1/2 activation and prevented H/R-induced apoptosis. Furthermore, blockade of JNK1/2 signaling inhibited apoptosis following H/R. The role of calpain in ER stress was also demonstrated in an in vivo model of ischemia/reperfusion using transgenic mice over-expressing calpastatin. In summary, calpain-1 induces ER stress and JNK1/2 activation, thereby mediating apoptosis in cardiomyocytes. Accordingly, inhibition of calpain prevents ER stress, JNK1/2 activation and apoptosis in H/R-induced cardiomyocytes. Thus, ER stress/JNK1/2 activation may represent an important mechanism linking calpain-1 to ischemic injury.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease - Volume 1852, Issue 5, May 2015, Pages 882-892
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease - Volume 1852, Issue 5, May 2015, Pages 882-892
نویسندگان
Dong Zheng, Grace Wang, Shuai Li, Guo-Chang Fan, Tianqing Peng,