INO80E Suppresses Oxidized LDL-Induced Endothelial Apoptosis Through HDAC1-Mediated Stabilization of YY1.
T, L., Q, L., S, Y., D, Y., X, L., L, Z., & Q, T. (2026). INO80E Suppresses Oxidized LDL-Induced Endothelial Apoptosis Through HDAC1-Mediated Stabilization of YY1.. Biomolecules. https://doi.org/10.3390/biom16081174
T L, Q L, S Y, D Y, X L, L Z, et al. INO80E Suppresses Oxidized LDL-Induced Endothelial Apoptosis Through HDAC1-Mediated Stabilization of YY1.. Biomolecules. 2026; doi: 10.3390/biom16081174
T L, Q L, S Y, et al. INO80E Suppresses Oxidized LDL-Induced Endothelial Apoptosis Through HDAC1-Mediated Stabilization of YY1.[J]. Biomolecules. 2026. DOI: 10.3390/biom16081174.
@article{t2026,
author = {Liu T and Luo Q and Yang S and Yang D and Lv X and Zhao L and Tuo Q},
title = {INO80E Suppresses Oxidized LDL-Induced Endothelial Apoptosis Through HDAC1-Mediated Stabilization of YY1.},
journal = {Biomolecules},
year = {2026},
doi = {10.3390/biom16081174},
note = {PMID: 42650841},
}
TY - JOUR AU - Liu T AU - Luo Q AU - Yang S AU - Yang D AU - Lv X AU - Zhao L AU - Tuo Q TI - INO80E Suppresses Oxidized LDL-Induced Endothelial Apoptosis Through HDAC1-Mediated Stabilization of YY1. T2 - Biomolecules PY - 2026 DO - 10.3390/biom16081174 AN - PMID:42650841 ER -
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.