Disruption of SM22 promotes inflammation after artery injury via nuclear factor kappaB activation.

ABSTRACT:

Rationale

SM22 (or transgelin), an actin-binding protein abundant in vascular smooth muscle cells (VSMCs), is downregulated in atherosclerosis, aneurysm and various cancers. Abolishing SM22 in apolipoprotein E knockout mice accelerates atherogenesis. However, it is unclear whether SM22 disruption independently promotes arterial inflammation.

Objective

To investigate whether SM22 disruption directly promotes inflammation on arterial injury and to characterize the underlying mechanisms.

Methods and results

Using carotid denudation as an artery injury model, we showed that Sm22 knockout (Sm22(-/-)) mice developed enhanced inflammatory responses with higher induction of proinflammatory genes, including Vcam1, Icam1, Cx3cl1, Ccl2, and Ptgs2. Higher expression of these gene

SUBMITTER: Shen J 

PROVIDER: S-EPMC2896867 | biostudies-literature | 2010 Apr

REPOSITORIES: biostudies-literature