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Aberrant endoplasmic reticulum stress mediates coronary artery spasm through regulating MLCK/MLC2 pathway 期刊论文

编号：

de24d34a-d073-42dc-8faf-0cefd9065910
作者：

Xue, Aimin^[1,2];Lin, Junyi(林俊毅)^[1]Que, Chunxing^[1];Yu, Yijing^[1];Tu, Chunyan^[1];Chen, Han^[1];Liu, Baonian(刘宝年)^[1]Zhao, Xin(赵昕)^[3]Wang, Tianhao^[4];Ma, Kaijun(马开军)^[2]Li, Liliang(李立亮)*^[1]
语种：

英文
期刊：

EXPERIMENTAL CELL RESEARCH ISSN：0014-4827 2018 年 363 卷 2 期 (321 - 331) ; FEB 15
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关键词：

Endoplasmic reticulum stress Coronary artery spasm MLCK/MLC2 pathway Vasoconstriction
摘要：

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.
推荐引用方式
GB/T 7714：

Xue Aimin,Lin Junyi,Que Chunxing, et al. Aberrant endoplasmic reticulum stress mediates coronary artery spasm through regulating MLCK/MLC2 pathway [J].EXPERIMENTAL CELL RESEARCH,2018,363(2):321-331.
APA：

Xue Aimin,Lin Junyi,Que Chunxing,Yu Yijing,&Li Liliang.(2018).Aberrant endoplasmic reticulum stress mediates coronary artery spasm through regulating MLCK/MLC2 pathway .EXPERIMENTAL CELL RESEARCH,363(2):321-331.
MLA：

Xue Aimin, et al. "Aberrant endoplasmic reticulum stress mediates coronary artery spasm through regulating MLCK/MLC2 pathway" .EXPERIMENTAL CELL RESEARCH 363,2(2018):321-331.
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