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Cell-free Biochemical Fluorometric Enzymatic Assay for High-throughput Measurement of Lipid Peroxidation in High Density Lipoprotein
Published on: October 12, 2017
INO80E Suppresses Oxidized LDL-Induced Endothelial Apoptosis Through HDAC1-Mediated Stabilization of YY1
Tingting Liu1,2,3, Quanye Luo3, Shihong Yang3
1Key Laboratory for Quality Evaluation of Bulk Herbs of Hunan Province, School of Pharmacy, Hunan University of Chinese Medicine, Changsha 410208, China.
Objectives:
Endothelial apoptosis is a central event in atherosclerotic vascular injury, yet the contribution of the INO80 chromatin-remodeling subunit INO80E to this process remains unclear. This study examined whether INO80E is altered during atherosclerosis (AS)-associated endothelial injury and explored its functional role in ox-LDL-triggered apoptosis.
Methods:
Atherosclerotic mouse models were used to examine INO80E expression in vascular tissues, and ox-LDL-treated HUVECs were applied as an in vitro model of endothelial injury. The functional role of INO80E was evaluated using lentiviral overexpression and siRNA-mediated knockdown approaches, while apoptosis was measured by flow cytometry and TUNEL staining. Mechanistic experiments included co-immunoprecipitation, immunofluorescence, YY1 acetylation analysis, and pharmacological inhibition with the pan-HDAC inhibitor trichostatin A (TSA). In addition, YY1-silencing rescue experiments were performed in INO80E-overexpressing cells to determine whether YY1 contributes to the protective effect of INO80E against ox-LDL-induced endothelial apoptosis.
Results:
INO80E expression was reduced in the endothelial layer of ApoE-/- aortas and in ox-LDL-treated HUVECs. INO80E overexpression attenuated ox-LDL-induced apoptosis and increased the Bcl-2/BAX ratio, whereas INO80E knockdown produced the opposite effect. INO80E colocalized with HDAC1, increased the HDAC1-YY1 association, decreased YY1 acetylation, and prolonged YY1 protein stability. TSA treatment weakened the anti-apoptotic phenotype associated with INO80E overexpression, and rescue experiments showed that YY1 knockdown partially reversed the INO80E overexpression-associated regulation of Bcl-2 and BAX.
Conclusions:
These findings suggest that INO80E protects endothelial cells from ox-LDL-induced apoptosis, at least in part by promoting HDAC-associated YY1 deacetylation and stabilization. The INO80E-HDAC1-YY1 pathway may represent a candidate protective mechanism in AS that requires further validation.
