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A role for FRNK, a selectively expressed inhibitor of focal adhesion kinase (FAK), in vascular growth and development

Focal adhesion kinase related non‐kinase (FRNK) is a dominant negative form of FAK that our group has previously shown to be selectively expressed in vascular smooth muscle cells (SMC). Here we aim to determine the function of FRNK in vivo and the mechanisms that regulate its SMC specific expression. Previously, we have shown that in primary cultured SMC, overexpression of FRNK attenuates PDGF‐mediated growth and migration. Our recent data reveals that FRNK expression is upregulated by the pro‐differentiation agonist TGF‐β and that over‐expression of FRNK enhances SMC differentiation marker gene expression in SMC. It has been shown that a 5kb region of the FRNK promoter sufficient for SMC specific promoter activity in vivo. We have identified two highly conserved 250bp segments of this promoter that are necessary and sufficient for SMC activity in vitro. Since we have shown that FRNK can modulate SMC phenotypes in cultured cells, we expected that FRNK deletion might cause overgrowth of SMC in vivo. FRNK−/ − and wild type mice have comparable aortic medial thickness, systolic blood pressure, and pressor response to phenylephrine. In response to carotid artery ligation, FRNK−/ − mice revealed decreased neointimal SMC marker gene expression 14 days following injury as compared to controls. These studies indicate that FRNK acts to control differentiation state of SMC in vivo.