scholarly journals Low Doses of Bisphenol A Promote Human Seminoma Cell Proliferation by Activating PKA and PKG via a Membrane G-Protein–Coupled Estrogen Receptor

2009 ◽  
Vol 117 (7) ◽  
pp. 1053-1058 ◽  
Author(s):  
Adil Bouskine ◽  
Marielle Nebout ◽  
Françoise Brücker-Davis ◽  
Mohamed Benahmed ◽  
Patrick Fenichel
Keyword(s):  
Cell Proliferation ◽  
Estrogen Receptor ◽  
Bisphenol A ◽  
G Protein ◽  
Low Doses ◽  
G Protein Coupled

scholarly journals SAT-LB035 The G Protein-Coupled Estrogen Receptor GPER Plays a Dominant Role in Human Islet Cell Proliferation upon High Glucose

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Sigal Shaklai ◽  
Meital Grafi-Cohen ◽  
Orli Sharon ◽  
Gabi Shefer ◽  
Dalia Somjen ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Estrogen Receptor ◽  
G Protein ◽  
High Glucose ◽  
Islet Cell ◽  
Dominant Role ◽  
Human Islet ◽  
G Protein Coupled

Abstract 1305: Activation of G-protein coupled estrogen receptor (GPER) inhibits ELT-3 uterine leiomyoma cell proliferation.

2013 ◽  
Author(s):  
Maryann Castillo ◽  
Angelique M. Wimbley ◽  
Jacob J. Mayfield ◽  
Jenifer C. Lascano ◽  
Kevin D. Houston
Keyword(s):  
Cell Proliferation ◽  
Estrogen Receptor ◽  
G Protein ◽  
Uterine Leiomyoma ◽  
G Protein Coupled

Activation of G protein–coupled estrogen receptor protects intestine from ischemia/reperfusion injury in mice by protecting the crypt cell proliferation

2019 ◽  
Vol 133 (3) ◽  
pp. 449-464 ◽  
Author(s):  
Shiquan Chai ◽  
Kaixuan Liu ◽  
Wanbing Feng ◽  
Tiantian Liu ◽  
Qian Wang ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cell Proliferation ◽  
Estrogen Receptor ◽  
G Protein ◽  
Ischemia Reperfusion ◽  
Inos Expression ◽  
Crypt Cell ◽  
Clinical Event ◽  
Crypt Cell Proliferation ◽  
G Protein Coupled

AbstractThe intestinal ischemia/reperfusion (I/R) injury is a common clinical event related with high mortality in patients undergoing surgery or trauma. Estrogen exerts salutary effect on intestinal I/R injury, but the receptor type is not totally understood. We aimed to identify whether the G protein–coupled estrogen receptor (GPER) could protect the intestine against I/R injury and explored the mechanism. Adult male C57BL/6 mice were subjected to intestinal I/R injury by clamping (45 min) of the superior mesenteric artery followed by 4 h of intestinal reperfusion. Our results revealed that the selective GPER blocker abolished the protective effect of estrogen on intestinal I/R injury. Selective GPER agonist G-1 significantly alleviated I/R-induced intestinal mucosal damage, neutrophil infiltration, up-regulation of TNF-α and cyclooxygenase-2 (Cox-2) expression, and restored impaired intestinal barrier function. G-1 could ameliorate the impaired crypt cell proliferation ability induced by I/R and restore the decrease in villus height and crypt depth. The up-regulation of inducible nitric oxide synthase (iNOS) expression after I/R treatment was attenuated by G-1 administration. Moreover, selective iNOS inhibitor had a similar effect with G-1 on promoting the proliferation of crypt cells in the intestinal I/R model. Both GPER and iNOS were expressed in leucine-rich repeat containing G-protein coupled receptor 5 (Lgr5) positive stem cells in crypt. Together, these findings demonstrate that GPER activation can prompt epithelial cell repair following intestinal injury, which occurred at least in part by inhibiting the iNOS expression in intestinal stem cells (ISCs). GPER may be a novel therapeutic target for intestinal I/R injury.

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