FASEB J 2016 Feb 14;30(2):702-15. Epub 2015 Oct 14.
*Vascular Biology Research Centre, Institute of Cardiovascular and Cell Sciences, and Institute of Medical and Biomedical Education, St. George's, University of London, London, United Kingdom; and Laboratory of Neurobiology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA.
Depletion of sarcoplasmic reticulum (SR) Ca(2+) stores activates store-operated channels (SOCs) composed of canonical transient receptor potential (TRPC) 1 proteins in vascular smooth muscle cells (VSMCs), which contribute to important cellular functions. We have previously shown that PKC is obligatory for activation of TRPC1 SOCs in VSMCs, and the present study investigates if the classic phosphoinositol signaling pathway involving Gαq-mediated PLC activity is responsible for driving PKC-dependent channel gating. The G-protein inhibitor GDP-β-S, anti-Gαq antibodies, the PLC inhibitor U73122, and the PKC inhibitor GF109203X all inhibited activation of TRPC1 SOCs, and U73122 and GF109203X also reduced store-operated PKC-dependent phosphorylation of TRPC1 proteins. Read More