کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8451392 | 1547694 | 2018 | 19 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Aberrant endoplasmic reticulum stress mediates coronary artery spasm through regulating MLCK/MLC2 pathway
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
5-HTdouble-stranded RNA-activated protein kinase (PKR)-like ER kinaseMLC2Myosin II regulatory light chainMLCKVSMCs4-PBAtunicamycinATF6inositol requiring enzyme 1IRE1UPRCASqRT-PCRvasoconstriction - انقباض عروق5-hydroxy tryptamine - 5 هیدروکسی تریپتامینACh - آهEndoplasmic reticulum stress - استرس شبکه آندوپلاسمیAcetylcholine - استیل کولینCoronary artery spasm - اسپاسم عروق کرونرelectrocardiograph - الکتروکاردیوگرافیECG - الکتروکاردیوگرام یا نوار قلبmyosin light chain kinase - زنجیره کیناز سبک مایوسینVascular smooth muscle cells - سلول های عضلانی صاف عروقیendoplasmic reticulum - شبکه آندوپلاسمی activating transcription factor 6 - فعال کردن عامل رونویسی 6quantitative real-time polymerase chain reaction - واکنش زنجیره ای پلیمراز کمی زمان واقعی استPERK - پرک
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
تحقیقات سرطان
پیش نمایش صفحه اول مقاله

چکیده انگلیسی
Coronary artery spasm (CAS) is a pathophysiological phenomenon that may cause myocardial infarction and lead to circulatory collapse and death. Aberrant endoplasmic reticulum (ER) stress causes accumulation of misfolding proteins and has been reported to be involved in a variety of vascular diseases. The present study investigated the role of ER stress in the development of CAS and explored the possible molecular mechanisms. Initially, it was found that ER stress markers were elevated in response to drug-induced vascular smooth muscle cells (VSMCs) contraction. Pharmacologic activation of ER stress using Tunicamycin (Tm) persistently induced CAS and significantly promoted Pituitrin-induced CAS in mice as well as in a collagen gel contraction assay. On the contrary, pharmacologic inhibition of ER stress using 4-phenylacetic acid (4-PBA) completely blunted Pituitrin-induced CAS development in mice. Moreover, during the drug-induced VSMCs contraction, expression of ER stress markers were increased in parallel to those of myosin light chain kinase (MLCK) and phosphor-MLC2 (p-MLC2, at Ser19). After inhibiting MLCK activity by using its specific inhibitor ML-7, the ER stress activator Tm failed to activate the MLCK/MLC2 pathway and could neither trigger CAS in mice nor induce VSMCs contraction in vitro. Our results suggested that aberrant ER stress mediated CAS via regulating the MLCK/MLC2 pathway. ER stress activators might be more robust than the common drugs (Pituitrin or acetylcholine) as to induce vasocontraction and thus may serve as potential therapeutics against chronic bleeding, while its inhibitor might be useful for treatment of severe CAS caused by other medication.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Experimental Cell Research - Volume 363, Issue 2, 15 February 2018, Pages 321-331
Journal: Experimental Cell Research - Volume 363, Issue 2, 15 February 2018, Pages 321-331
نویسندگان
Aimin Xue, Junyi Lin, Chunxing Que, Yijing Yu, Chunyan Tu, Han Chen, Baonian Liu, Xin Zhao, Tianhao Wang, Kaijun Ma, Liliang Li,