HDAC9 regulates ox-LDL-induced endothelial cell apoptosis by participating in inflammatory reactions.
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-alpha 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.
Department of Neurology, Huashan Hospital, State Key Laboratory of Medical Neurobiology of Fudan University, Shanghai, 200040, China.
Xu
X
Han
Department of Neurology, Huashan Hospital, State Key Laboratory of Medical Neurobiology of Fudan University, Shanghai, 200040, China.
Xiang
X
Han
Department of Neurology, Huashan Hospital, State Key Laboratory of Medical Neurobiology of Fudan University, Shanghai, 200040, China.
Zheng
Z
Wang
Department of Rehabilitatipn, Suzhou Municipal Hospital, No.26 Daoqian Road, Suzhou, Jiangsu, 215000, China.
Junjun
J
Shen
Department of Neurology, Huashan Hospital, state key laboratory of medical neurobiology of Fudan University, Shanghai, 200040, China, qiang_dong163@yeah.net.
Qiang
Q
Dong
D017209:Apoptosis / Q000502:physiology*; D050197:Atherosclerosis / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D002470:Cell Survival; D002478:Cells, Cultured; D055785:Gene Knockdown Techniques; D006655:Histone Deacetylases / Q000235:genetics / Q000378:metabolism*; D061307:Human Umbilical Vein Endothelial Cells / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D007249:Inflammation / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D018836:Inflammation Mediators / Q000378:metabolism; D008077:Lipoproteins, LDL / Q000378:metabolism*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D034741:RNA, Small Interfering / Q000235:genetics; D012097:Repressor Proteins / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*
D018836:Inflammation Mediators; D008077:Lipoproteins, LDL; D012333:RNA, Messenger; D034741:RNA, Small Interfering; D012097:Repressor Proteins; C099252:oxidized low density lipoprotein; C486544:HDAC9 protein, human; D006655:Histone Deacetylases