Key result
TGFbeta-activated PKCdelta is critical to maintain normal expression of Smad3, which in turn is required for the induction of fibronectin in vascular smooth muscle cells.
Population
A10 rat aortic smooth muscle cells (SMCs) and aortic SMCs isolated from PKCdelta(-/-) mice
Comparison
Modulation of PKCdelta activity and Smad3/7… vs Control/untreated cells or wild-type cells
Design
Preclinical
Authors
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PKCdelta may be a target to limit vascular fibrosis after injury; animal data leave human translation open.
TGFbeta-activated PKCdelta is necessary for maintaining Smad3 expression and subsequent fibronectin synthesis in vascular smooth muscle cells, identifying PKCdelta as a potential target for fibroproliferative responses after arterial injury.
Ryer et al. (2006) studied Fibroproliferative response after arterial injury. PKCdelta inhibition or overexpression was evaluated on Fibronectin protein and mRNA expression. TGFbeta-activated PKCdelta is critical to maintain normal expression of Smad3, which in turn is required for the induction of fibronectin in vascular smooth muscle cells.
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