Reduction of PKCbetaII activity in smooth muscle cells attenuates acute arterial injury.

ABSTRACT:

Objective

The ubiquitous enzyme protein kinase C (PKC) has been linked to the pathogenesis of vascular injury, but the cell-specific and discrete functions of the betaII isoform have yet to be discovered in this setting. Our previous findings demonstrated significantly increased PKCbetaII in the membrane fraction of injured femoral arteries in wild type (WT) mice and revealed reduction of neointimal expansion in PKCbeta(-/-) mice after acute vascular injury. As PKCbeta(-/-) mice are globally devoid of PKCbeta, we established novel transgenic (Tg) mice to test the hypothesis that the action of PKCbetaII specifically in smooth muscle cells (SMCs) mediates the formation of neointimal lesions in response to arterial injury.

Methods

Tg mice expressing SM22alpha promoter-targeted

SUBMITTER: Huang C 

PROVIDER: S-EPMC3138398 | biostudies-literature | 2010 Sep

REPOSITORIES: biostudies-literature