Angiotensin II-induced histone deacetylase 5 phosphorylation, nuclear export, and Egr-1 expression are mediated by Akt pathway in A10 vascular smooth muscle cells
Vanessa Truong, Ashish Jain, Madhu B. Anand‐Srivastava, Ashok K. Srivastava
Abstract
ANG II-induced histone deacetylase 5 (HDAC5) phosphorylation and nuclear export occurs via the phosphoinositide 3-kinase/Akt pathway. Akt, through HDAC5, regulates ANG II-induced expression of early growth response protein-1 (Egr-1), which is a transcription factor linked with vascular dysfunction. Inhibition of HDAC5 exclusion by nuclear export inhibitors suppresses ANG II-induced Egr-1 expression. HDAC5 is an upstream mediator of Egr-1 expression and cell hypertrophy in response to ANG II in vascular smooth muscle cells.
Topics & Concepts
Histone deacetylase 5Protein kinase BHistone deacetylasePhosphorylationAngiotensin IICell biologyHistone deacetylase 2PI3K/AKT/mTOR pathwayVascular smooth muscleChemistryNuclear export signalNuclear transportTranscription factorSignal transductionBiologyHistoneCancer researchEndocrinologyCell nucleusCytoplasmBiochemistryGeneBlood pressureSmooth muscleNuclear Receptors and SignalingGDF15 and Related BiomarkersRenin-Angiotensin System Studies