自噬
内质网
糖皮质激素
细胞生物学
未折叠蛋白反应
细胞凋亡
信号转导
程序性细胞死亡
化学
生物
免疫学
生物化学
作者
Yanchun Gao,Hongyi Zhu,Fan Yang,Qiyang Wang,Yong Feng,Changqing Zhang
出处
期刊:American Journal of Physiology-cell Physiology
[American Physical Society]
日期:2018-05-16
卷期号:315 (3): C300-C309
被引量:10
标识
DOI:10.1152/ajpcell.00009.2018
摘要
Glucocorticoid-induced endothelial injury has been reported in several diseases. Although there are several theories, the exact mechanism underlying the role of glucocorticoids in this process remains unclear. Autophagy has been reported to occur as a response to different stimuli and can affect cell survival and function. In this study, we found that glucocorticoids induced apoptosis and endoplasmic reticulum (ER) stress in endotheliocytes. Furthermore, we discovered that glucocorticoids induced autophagy in these cells and the inositol requiring protein 1 (IRE1α)/X-box binding protein 1s (XBP-1s) axis, one of the downstream signaling pathways of ER stress, was associated with the glucocorticoid-induced autophagy. The autophagy partly protected endotheliocytes from glucocorticoid-induced apoptosis and inhibition of proliferation. In conclusion, glucocorticoid-induced endoplasmic reticulum stress activated the IRE1α/XBP-1s signaling and induced autophagy, which, in turn, played a protective role in endotheliocyte survival and proliferation, avoiding further cellular damage caused by glucocorticoids.
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