Title : G Protein-Coupled Estrogen Receptor 1 Mediates Acute Estrogen-Induced Cardioprotection via MEK/ERK/GSK-3β Pathway after Ischemia/Reperfusion.

Pub. Date : 2015

PMID : 26356837






4 Functional Relationships(s)
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1 Inhibition of MEK1/2/ERK1/2 (1 muM U0126) and PI-3K/Akt (10 muM LY294002) signaling showed that the MEK1/2/ERK1/2 pathway via GSK-3beta exclusively was responsible for cardioprotection as an addition of U0126 prevented estrogen-induced GSK-3beta increased phosphorylation, resistance to mitochondrial Ca2+-overload, functional recovery and protection against infarction. U 0126 mitogen-activated protein kinase kinase 1 Mus musculus
2 Inhibition of MEK1/2/ERK1/2 (1 muM U0126) and PI-3K/Akt (10 muM LY294002) signaling showed that the MEK1/2/ERK1/2 pathway via GSK-3beta exclusively was responsible for cardioprotection as an addition of U0126 prevented estrogen-induced GSK-3beta increased phosphorylation, resistance to mitochondrial Ca2+-overload, functional recovery and protection against infarction. U 0126 mitogen-activated protein kinase kinase 1 Mus musculus
3 Inhibition of MEK1/2/ERK1/2 (1 muM U0126) and PI-3K/Akt (10 muM LY294002) signaling showed that the MEK1/2/ERK1/2 pathway via GSK-3beta exclusively was responsible for cardioprotection as an addition of U0126 prevented estrogen-induced GSK-3beta increased phosphorylation, resistance to mitochondrial Ca2+-overload, functional recovery and protection against infarction. U 0126 mitogen-activated protein kinase kinase 1 Mus musculus
4 Inhibition of MEK1/2/ERK1/2 (1 muM U0126) and PI-3K/Akt (10 muM LY294002) signaling showed that the MEK1/2/ERK1/2 pathway via GSK-3beta exclusively was responsible for cardioprotection as an addition of U0126 prevented estrogen-induced GSK-3beta increased phosphorylation, resistance to mitochondrial Ca2+-overload, functional recovery and protection against infarction. U 0126 mitogen-activated protein kinase kinase 1 Mus musculus