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See Latest ArticlesA novel estrogen receptor GPER inhibits mitochondria permeability transition pore opening and protects the heart against ischemia/reperfusion injury
Heart And Circulatory Physiology, 11/03/09
Bopassa JC et al. – The results suggest that GPER activation provide a cardioprotective effect after ischemia–reperfusion by inhibiting the mPTP opening and this effect is mediated by Erk pathway.
Jean Chrisostome Bopassa, 11/03/09
| It is my pleasure to do this work in Stefani's lab at UCLA, Department of Anesthesiology. I think you will have a real pleasure to read this paper. Any feedback will be welcomed. I want to thank Dr Stefani, Dr Toro and Dr Eghbali for their contribution to this work. Our goal in the lab is to determine the role and mechanism of estrogen in cardioprotection. The current study allows better understanding estrogen rapid action. It is clear that one of the receptor mediated the rapid action of estrogen is GPER. The activation of this receptor by estrogen or G1 (a specific agonist) leads to the inhibition of the mitochondrial permeability transition pore opening. Therefore preventing massive calcium uptake by mitochondria, which is involved in cardioprotection. Our work shows also that Erk phosphorylation is a main mediator of this action, indicating the involving of MERK pathway. Thank you for your time to read this paper. Regards, Dr Jean Chrisostome Bopassa jbopassa@hotmail.com |
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