Premium
Loss of function of CaV1.2 in cultured bovine coronary artery smooth muscle cells
Author(s) -
Ochi Rikuo,
Gupte Rakhee S,
Abe Madoka,
Murayama Takashi,
Kurebayashi Nagomi,
Gupte Sachin A
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.1018.9
Subject(s) - transfection , vascular smooth muscle , western blot , microbiology and biotechnology , hek 293 cells , protein subunit , cell culture , cav1.2 , contraction (grammar) , myocyte , chemistry , biology , smooth muscle , endocrinology , biochemistry , gene , genetics
L‐type Ca 2+ current ( I Ca,L ) through Cav1.2 α subunit pore controls contraction and phenotype change between contractile and proliferative type in vascular smooth muscle cell (VSMC). I Ca,L enhances the expression of proteins that are characteristic for contractile phenotype. I Ca,L is small in proliferative VSMC. The phenotype change to proliferative type is involved in atherogenesis. To explore underlying mechanism of the reduction of I Ca,L reduction in proliferative VSMC, we have compared (1) the density of I Ca,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 I Ca,L was recorded with 10 mM Ba 2+ as the charge carrier. I Ca,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. I Ca,L density was 4.2±0.7 pA/PF (n=15) in HEK293 cells transfected with human cardiac CaV1.2α‐GFP . However, I Ca,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 I Ca,L in the proliferatative vascular smooth muscle cells. This study is supported by NIH grant#R01HL85352