Publication: Epac is required for GLP-1R-mediated inhibition of oxidative stress and apoptosis in cardiomyocytes
Issued Date
2015-01-01
Resource Type
ISSN
19449917
08888809
08888809
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2-s2.0-84926335902
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Mahidol University
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SCOPUS
Bibliographic Citation
Molecular Endocrinology. Vol.29, No.4 (2015), 583-596
Suggested Citation
Supachoke Mangmool, Piriya Hemplueksa, Warisara Parichatikanond, Nipon Chattipakorn Epac is required for GLP-1R-mediated inhibition of oxidative stress and apoptosis in cardiomyocytes. Molecular Endocrinology. Vol.29, No.4 (2015), 583-596. doi:10.1210/me.2014-1346 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/35581
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Title
Epac is required for GLP-1R-mediated inhibition of oxidative stress and apoptosis in cardiomyocytes
Abstract
© 2015 by the Endocrine Society. Although the cardioprotective effects of glucagon-like peptide-1 and its analogs have been reported, the exact mechanisms of the glucagon-like peptide-1 receptor (GLP-1R) signaling pathway in the heart are still unclear. Activation of the GLP-1R has been shown to increase cAMP levels, thus eliciting protein kinase A- and exchange protein activated by cAMP (Epac)-dependent signaling pathways in pancreatic b-cells. However, which pathway plays an important role in the antioxidant and antiapoptotic effects of GLP-1R activation in the heart is not known. In this study, we demonstrated that stimulation of GLP-1Rs with exendin-4 attenuated H2O2-induced reactive oxygen species production and increased the synthesis of antioxidant enzymes, catalase, glutathione peroxidase-1, and manganese superoxide dismutase that is dependent on Epac. Additionally, exendin-4 has an antiapoptotic effect by decreasing a number of apoptotic cells, inhibiting caspase-3 activity, and enhancing the expression of antiapoptotic protein B-cell lymphoma 2, which is mediated through both protein kinase A- and Epac-dependent pathways. These data indicate a critical role for Epac in GLP-1R-mediated cardioprotection.