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Both GPER and membrane oestrogen receptor-α activation protect ventricular remodelling in 17β oestradiol-treated ovariectomized infarcted rats.

Lee TM, Lin SZ, Chang NC - J. Cell. Mol. Med. (2014)

Bottom Line: We investigated whether the attenuated hypertrophic effect of oestradiol was via activation of phosphatidylinositol 3-kinase (PI3K)/Akt/endothelial nitric oxide synthase (eNOS) through non-genomic action.The specific PI3K inhibitor, LY290042, completely abolished Akt activation and eNOS phosphorylation in infarcted hearts treated with either oestradiol or oestradiol + G-15.These data support the conclusions that oestradiol improves ventricular remodelling by both GPER- and membrane-bound ERα-dependent mechanisms that converge into the PI3K/Akt/eNOS pathway, unveiling a novel mechanism by which oestradiol regulates pathological cardiomyocyte growth after infarction.

View Article: PubMed Central - PubMed

Affiliation: Department of Medicine, Cardiology Section, China Medical University-An Nan Hospital, Tainan, Taiwan; Department of Medicine, China Medical University, Taichung, Taiwan; Department of Internal Medicine, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.

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Reaction sequences leading to attenuated cardiomyocyte hypertrophy after infarction. The diagram summarizes the anatomical, molecular and pharmacological evidence presented in this report. Inhibition of these signalling pathways by their respective inhibitors is indicated by the vertical lines.
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fig07: Reaction sequences leading to attenuated cardiomyocyte hypertrophy after infarction. The diagram summarizes the anatomical, molecular and pharmacological evidence presented in this report. Inhibition of these signalling pathways by their respective inhibitors is indicated by the vertical lines.

Mentions: The present study illustrates an additional role for E2, showing that both GPER and membrane-bound ERα signallings are operative to improve ventricular remodelling through a common PI3K/Akt/eNOS-dependent pathway. The beneficial effect of E2 on the ventricular remodelling was supported by the following evidence (Fig. 7):


Both GPER and membrane oestrogen receptor-α activation protect ventricular remodelling in 17β oestradiol-treated ovariectomized infarcted rats.

Lee TM, Lin SZ, Chang NC - J. Cell. Mol. Med. (2014)

Reaction sequences leading to attenuated cardiomyocyte hypertrophy after infarction. The diagram summarizes the anatomical, molecular and pharmacological evidence presented in this report. Inhibition of these signalling pathways by their respective inhibitors is indicated by the vertical lines.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4302651&req=5

fig07: Reaction sequences leading to attenuated cardiomyocyte hypertrophy after infarction. The diagram summarizes the anatomical, molecular and pharmacological evidence presented in this report. Inhibition of these signalling pathways by their respective inhibitors is indicated by the vertical lines.
Mentions: The present study illustrates an additional role for E2, showing that both GPER and membrane-bound ERα signallings are operative to improve ventricular remodelling through a common PI3K/Akt/eNOS-dependent pathway. The beneficial effect of E2 on the ventricular remodelling was supported by the following evidence (Fig. 7):

Bottom Line: We investigated whether the attenuated hypertrophic effect of oestradiol was via activation of phosphatidylinositol 3-kinase (PI3K)/Akt/endothelial nitric oxide synthase (eNOS) through non-genomic action.The specific PI3K inhibitor, LY290042, completely abolished Akt activation and eNOS phosphorylation in infarcted hearts treated with either oestradiol or oestradiol + G-15.These data support the conclusions that oestradiol improves ventricular remodelling by both GPER- and membrane-bound ERα-dependent mechanisms that converge into the PI3K/Akt/eNOS pathway, unveiling a novel mechanism by which oestradiol regulates pathological cardiomyocyte growth after infarction.

View Article: PubMed Central - PubMed

Affiliation: Department of Medicine, Cardiology Section, China Medical University-An Nan Hospital, Tainan, Taiwan; Department of Medicine, China Medical University, Taichung, Taiwan; Department of Internal Medicine, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.

Show MeSH
Related in: MedlinePlus