GIT1 mediates HDAC5 activation by angiotensin II in vascular smooth muscle cells.

ABSTRACT:

Objective

The G protein-coupled receptor (GPCR)-kinase2 interacting protein1 (GIT1) is a scaffold protein involved in angiotensin II (Ang II) signaling. Histone deacetylase-5 (HDAC5) has emerged as an important substrate of calcium/calmodulin-dependent protein kinase II (CamK II) in GPCR signaling. Here we investigated the hypothesis that Ang II-mediated vascular smooth muscle cell (VSMC) gene transcription involves GIT1-CamK II-dependent phosphorylation of HDAC5.

Methods and results

Ang II rapidly stimulated phosphorylation of HDAC5 at Ser498 in VSMCs. Knockdown of GIT1 significantly decreased HDAC5 phosphorylation induced by Ang II. The involvement of Src, phospholipase gamma (PLCgamma), and CamK II in GIT1-mediated HDAC5 phosphorylation was demonstrated. The association o

SUBMITTER: Pang J 

PROVIDER: S-EPMC2735338 | biostudies-literature | 2008 May

REPOSITORIES: biostudies-literature