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TRPC6 and Orai1 expression increase with mitogen augmented store‐operated Ca 2+ entry in rat aortic smooth muscle
Author(s) -
Emter Craig A.,
Shaw Rebecca L.,
Bowles Douglas K.
Publication year - 2008
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.22.1_supplement.965.3
Subject(s) - trpc6 , orai1 , trpc , stim1 , chemistry , platelet derived growth factor receptor , voltage dependent calcium channel , microbiology and biotechnology , platelet derived growth factor , endocrinology , medicine , transient receptor potential channel , receptor , growth factor , biology , calcium , biochemistry , endoplasmic reticulum
Transient receptor potential canonical (TRPC), Orai1, and STIM1 proteins are proposed components of store‐operated Ca 2+ (SOC) channels. Increases in SOC entry (SOCE) may play a role in phenotype modulation of smooth muscle cells via Ca 2+ ‐dependent signaling mechanisms. The purpose of this study was to determine if mitogen‐induced phenotype modulation alters SOCE or expression of components comprising SOC channels. 24 hour treatment of cultured rat aortic smooth muscle cells (RASMC) with platelet‐derived growth factor‐BB (PDGF‐BB) increased intracellular Ca 2+ levels and rate of SOCE (p<0.05) induced by 10 minute exposure to 10 μM cyclopiazonic acid (CPA). CPA exposure increased SOC currents (I SOC ) in the PDGF‐BB treatment group and reversal potential shifted from 0 mV to approximately +10 mV (whole‐cell voltage clamp). TRPC6 and Orai1 protein and mRNA expression increased (p<0.05) and STIM1 decreased (p<0.05) in PDGF‐BB treated RASMC. Our results show treatment with PDGF‐BB increases SOCE and I SOC in cultured RASMC with concurrent increases in TRPC6 and Orai1 and decreased STIM1 expression. In conclusion, increased SOCE is characteristic of mitogen‐induced phenotype modulation in RASMC. We speculate that a TRPC6‐Orai1 complex may form the components of the SOC channel following PDGF‐BB treatment. Research support: NIH HL52490.