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Regulation of Store‐Operated Ca2+ Entry in the Vascular Endothelium by the G Protein‐Coupled Estrogen Receptor
Author(s) -
Terry Lara,
TRAN KIM,
VerMeer Mark,
Giles Jennifer
Publication year - 2013
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.27.1_supplement.lb511
Subject(s) - gper , microbiology and biotechnology , chemistry , estrogen receptor , stim1 , receptor , stromal cell , g protein coupled receptor , medicine , biology , biochemistry , endoplasmic reticulum , cancer research , cancer , breast cancer
The novel G protein‐coupled estrogen receptor (GPER/GPR30) has been found to participate in numerous cardiovascular functions. Store‐operated Ca 2+ entry (SOCE) is an essential mechanism that is required for many endothelial cell functions. We found that activation of GPER using the GPER specific agonist G1 is associated with a dose‐dependent inhibition of SOCE in primary vascular endothelial cells. Interestingly, the GPER specific antagonist G15 increases SOCE in cells unstimulated by GPER intrinsic or exogenous ligand. Overexpression of GPER in HEK 293 cells is associated with a 40% decrease in the rate of SOCE, while knockdown of GPER in endothelial cells using shRNA or antisense oligomer directed against GPER increases SOCE by approximately 50%. In addition, coimmunoprecipitation revealed that GPER exists in endothelial cells as a glycosylated protein and forms a complex with the stromal interaction molecule 1 (Stim1). These data suggest that GPER may be an important regulatory input of store‐operated Ca 2+ entry via its interaction with Stim1.