Transforming growth factor beta up-regulates cysteine-rich protein 2 in vascular smooth muscle cells via activating transcription factor 2.

ABSTRACT: CRP2 (cysteine-rich protein) is a vascular smooth muscle cell (VSMC)-expressed LIM-only protein. CRP2 associates with the actin cytoskeleton and interacts with transcription factors in the nucleus to mediate smooth muscle cell gene expression. Using Csrp2 (gene symbol of the mouse CRP2 gene)-deficient mice, we previously demonstrated that an absence of CRP2 enhances VSMC migration and increases neointima formation following arterial injury. Despite its importance in vascular injury, the molecular mechanisms controlling CRP2 expression in VSMC are largely unknown. Transforming growth factor beta (TGFbeta), a key factor present in the vessel wall in the early phases of arterial response to injury, plays an important role in modulating lesion formation. Because both CRP2 and TGFbeta are media

SUBMITTER: Lin DW 

PROVIDER: S-EPMC2397482 | biostudies-literature | 2008 May

REPOSITORIES: biostudies-literature