Open AccessAngiotensin II Stimulates Protein Kinase D-Dependent Histone Deacetylase 5 Phosphorylation and Nuclear Export Leading to Vascular Smooth Muscle Cell Hypertrophy
Author(s) -
Xiangbin Xu,
Chang Hoon Ha,
Chelsea Wong,
Weiye Wang,
Angelika Haußer,
Klaus Pfizenmaier,
Eric N. Olson,
Timothy A. McKinsey,
Zheng-Gen Jin
Publication year - 2007
Publication title -
arteriosclerosis thrombosis and vascular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.007
H-Index - 270
eISSN - 1524-4636
pISSN - 1079-5642
DOI - 10.1161/atvbaha.107.151704
Subject(s) - histone deacetylase 5 , mef2 , hdac4 , endocrinology , angiotensin ii , medicine , phosphorylation , biology , vascular smooth muscle , signal transduction , histone deacetylase , muscle hypertrophy , microbiology and biotechnology , histone , biochemistry , enhancer , transcription factor , smooth muscle , gene , blood pressure
Angiotensin II (Ang II) induces the phenotypic modulation and hypertrophy of vascular smooth muscle cells (VSMCs), which is implicated in the pathogenesis of hypertension, atherosclerosis, and diabetes. In this study, we tested the hypothesis that histone deacetylases 5 (HDAC5) and its signal pathway play a role in Ang II-induced VSMC hypertrophy.
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