Response gene to complement 32 promotes vascular lesion formation through stimulation of smooth muscle cell proliferation and migration.

ABSTRACT:

Objective

The objectives of this study were to determine the role of response gene to complement 32 (RGC-32) in vascular lesion formation after experimental angioplasty and to explore the underlying mechanisms.

Methods and results

Using a rat carotid artery balloon-injury model, we documented for the first time that neointima formation was closely associated with a significantly increased expression of RGC-32 protein. Short hairpin RNA knockdown of RGC-32 via adenovirus-mediated gene delivery dramatically inhibited the lesion formation by 62% as compared with control groups 14 days after injury. Conversely, RGC-32 overexpression significantly promoted the neointima formation by 33%. Gain- and loss-of-function studies in primary culture of rat aortic smooth muscle cells (RASM

SUBMITTER: Wang JN 

PROVIDER: S-EPMC3146015 | biostudies-literature | 2011 Aug

REPOSITORIES: biostudies-literature