HDAC9 regulates ox-LDL-induced endothelial cell apoptosis by participating in inflammatory reactions (original) (raw)

IMR Press / FBL / Volume 21 / Issue 5 / DOI: 10.2741/4428

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Article

Affiliation

1 Department of Neurology, Huashan Hospital, State Key Laboratory of Medical Neurobiology of Fudan University, Shanghai, 200040, China

2 Department of Rehabilitatipn, Suzhou Municipal Hospital, No.26 Daoqian Road, Suzhou, Jiangsu, 215000, China

Abstract

Atherosclerosis is the most common cause of cardiovascular diseases worldwide. The endothelial cell apoptosis elicited by oxidized low-density lipoprotein (ox-LDL), which contributes to endothelial damage and inflammation, is a particularly important event in the early stage of atherosclerosis. However, the mechanism underlying ox-LDL-induced endothelial cell apoptosis remains unclear. Here we found that HDAC9 expression was increased at both the mRNA and protein levels accompanied by dose-dependent ox-LDL-induced endothelial cell apoptosis. Depletion of HDAC9 by its specific shRNA significantly antagonized ox-LDL-induced cell apoptosis and suppressed the expression of ox-LDL-induced inflammatory factors, such as TNF-α and MCP1. These data suggest that HDAC9 is an important epigenetic factor regulating ox-LDL-induced endothelial cell apoptosis and inflammatory factor expression. These results suggest that HDAC9 may participate in ox-LDL-induced endothelial damage and inflammation during atherosclerosis development.

Keywords

Ox-LDL

TNF-α

HUVECs

Front. Biosci. (Landmark Ed) Print ISSN 2768-6701 Electronic ISSN 2768-6698

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