G-protein coupled estrogen receptor 1 expression in rat and human heart : protective role during ischaemic stress
Patel, Vanlata H., Chen, Jing, Ramanjaneya, Manjunath, Karteris, Emmanouil, Zachariades, Elena, Thomas, Peter, Been, Martin and Randeva, Harpal S.. (2010) G-protein coupled estrogen receptor 1 expression in rat and human heart : protective role during ischaemic stress. International Journal of Molecular Medicine, Vol.26 (No.2). pp. 193-199. ISSN 1107-3756Full text not available from this repository.
Official URL: http://dx.doi.org/10.3892/ijmm_00000452
G-protein coupled estrogen receptor 1, GPER, formerly known as GPR30, is a seven transmembrane domain receptor that mediates rapid estrogen responses in a wide variety of cell types. To date, little is known about the role of GPER during ischaemia/reperfusion injury. In this study, we report both mRNA and protein expression of GPER in the rat and human heart. The role of GPER in estrogen protection against ischaemic stress in the rat heart was also assessed using the isolated Langendorff system. Pre-treatment with 17 beta-estradiol (E2) significantly decreased infarct size, (61.48 +/- 2.2% to 27.92 +/- 2.9% (P<0.001). Similarly, treatment with the GPER agonist G1 prior to 30-min global ischaemia followed by 120-min reperfusion significantly reduced infarct size from 61.48 +/- 2.2% to 23.85 +/- 3.2% (P<0.001), whilst addition of GPR30 antibody, abolished the protective effect of G1 (infarct size: 55.42 +/- 1.3%). The results suggest that GPER under cardiac stress exerts direct protection in the heart and may serve as a potential therapeutic target for cardiac drug therapy.
|Item Type:||Journal Article|
|Divisions:||Faculty of Medicine > Warwick Medical School > Biomedical Sciences > Translational & Experimental Medicine > Metabolic and Vascular Health (- until July 2016)
Faculty of Medicine > Warwick Medical School
|Journal or Publication Title:||International Journal of Molecular Medicine|
|Official Date:||August 2010|
|Number of Pages:||7|
|Page Range:||pp. 193-199|
|Access rights to Published version:||Restricted or Subscription Access|
|Funder:||John Kennedy Research Fund, National Institutes of Health|
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