Impaired lipophagy in endothelial cells with prolonged exposure to oxidized low‑density lipoprotein

内皮细胞长期暴露于氧化低密度脂蛋白会导致脂肪吞噬功能受损

阅读:4
作者:Cai-Ping Zhang #, Xin-Xin Ding #, Tian Tian #, Bo-Jie Li, Chu-Yao Wang, Su-Su Jiang, Jin-Qi Shao, Yu-Lin Yuan, Ying Tian, Min Zhang, Shi-Yin Long

Abstract

Oxidative stress induces the formation of oxidized low‑density lipoprotein (ox‑LDL), which accelerates the development of atherosclerosis and the rupture of atherosclerotic plaques by promoting lipid accumulation and inhibiting autophagy in vascular cells. Lipophagy is known to be involved in maintaining the balance of neutral lipid metabolism; however, the phenomenon of lipophagy deficiency in ox‑LDL‑treated endothelial cells (ECs) remains to be elucidated. It has been demonstrated that lipid accumulation caused by ox‑LDL inhibits autophagy, which promotes apoptosis in ECs. The aim of the present study was to investigate the association between decreased autophagy and lipid accumulation in ECs treated with ox‑LDL. Electron microscopy demonstrated that the formation of autolipophagosomes was decreased in ox‑LDL‑treated human umbilical vein ECs compared with that in the LDL‑treated group and was accompanied by a decrease in the autophagy‑associated proteins via western blotting analysis. Using laser focal colocalization detection, decreased lipid processing was observed in the lysosomes of ox‑LDL‑treated ECs, which indicated that lipophagy may be attenuated and subsequently result in lipid accumulation in ox‑LDL‑treated ECs.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。