HADC regulates the diabetic vascular endothelial dysfunction by targetting MnSOD.
Ontology highlight
ABSTRACT: Vascular dysfunction is a common result of diabetes in humans. However, the mechanism underlying diabetic vascular dysfunction is not fully understood. Here in the present study, we showed that the histone deacetylase 2 (HDAC2) promoted the endothelial dysfunction induced by diabetes. The expression and activity of HDAC2 were up-regulated in vascular endothelial cells (ECs) from diabetic patients and mice. The expression of HDAC2 was also increased by high glucose stress in isolated human ECs. HDAC2 knockdown repressed the proliferation rate and promoted high glucose-induced apoptosis of ECs, which was associated with the activation of apoptotic pathways (Bcl-2, Caspase 3, and Bax). By contrast, HDAC2 overexpression led to opposing results. Significantly, we observed that HDAC2 regu
SUBMITTER: Hou Q
PROVIDER: S-EPMC6165838 | biostudies-literature | 2018 Oct
REPOSITORIES: biostudies-literature
ACCESS DATA