Key result
HDAC9 depletion reduces ox-LDL-induced endothelial apoptosis and suppresses key inflammatory factors.
Why the study?
The mechanism underlying ox-LDL-induced endothelial cell apoptosis, a key event in early atherosclerosis, remains unclear.
Does depletion of HDAC9 prevent ox-LDL-induced endothelial cell apoptosis and inflammation?
Does depletion of HDAC9 prevent ox-LDL-induced endothelial cell apoptosis and inflammation?
HDAC9 depletion reduces ox-LDL-induced endothelial cell apoptosis and inflammation, highlighting its potential role as an epigenetic regulator in early atherosclerosis development.
May implicate HDAC9 in ox-LDL endothelial injury; leaves open therapeutic targeting in atherosclerosis.
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.
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A 2016 study studied Atherosclerosis. HDAC9 depletion by specific shRNA was evaluated on ox-LDL-induced cell apoptosis and expression of inflammatory factors. Depletion of HDAC9 by specific shRNA significantly antagonized ox-LDL-induced endothelial cell apoptosis and suppressed the expression of inflammatory factors such as TNF-alpha and MCP1.
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