Loss of function of CaV1.2 in cultured bovine coronary artery smooth muscle cells

Abstract

L‐type Ca2+ current (ICa,L) through Cav1.2 α subunit pore controls contraction and phenotype change between contractile and proliferative type in vascular smooth muscle cell (VSMC). ICa,L enhances the expression of proteins that are characteristic for contractile phenotype. ICa,L is small in proliferative VSMC. The phenotype change to proliferative type is involved in atherogenesis. To explore underlying mechanism of the reduction of ICa,L reduction in proliferative VSMC, we have compared (1) the density of ICa,L between freshly‐isolated and proliferative cultured bovine coronary artery smooth muscle cell (BCASMC) and (2) the effect of CaV1.2 α subunit transfection to cultured BCASMC and HEK293 cells. Whole cell ICa,L was recorded with 10 mM Ba2+ as the charge carrier. ICa,L was 3.0 ± 0.4 pA/pF (n=28) in freshly isolated BCASMC but was not detectable in cultured BCASMC (N=15). Significant expression of CaV1.2 α subunit was confirmed by western blot in cultured BCASMC. ICa,L density was 4.2±0.7 pA/PF (n=15) in HEK293 cells transfected with human cardiac CaV1.2α‐GFP. However, ICa,L was not detectable in cultured BCASMC with the same transfection (n=15). We conclude that loss of function of expressed CaV1.2 is responsible for the reduction of ICa,L in the proliferatative vascular smooth muscle cells. This study is supported by NIH grant#R01HL85352