EdCC reduces myocardial ischemia-reperfusion injury via MEK-ERK signaling pathway
10.3969/j.issn.1000-4718.2016.02.005
- VernacularTitle:EdCC通过MEK-ERK信号通路减轻小鼠心肌缺血再灌注损伤
- Author:
Zhi JIANG
;
Zhongshen JIA
;
Yueting WU
;
Fang WEI
- Publication Type:Journal Article
- Keywords:
Endometrial stem cell-derived cytokine cocktail;
MEK-ERK signaling pathway;
Myocardial in-farction;
Ischemia-eperfusion injury
- From:
Chinese Journal of Pathophysiology
2016;32(2):221-227
- CountryChina
- Language:Chinese
-
Abstract:
AIM:To investigate the myocardial protective effect of endometrial stem cell ( EnSC)-derived cyto-kine cocktail ( EdCC) on myocardial ischemic reperfusion injury and the MEK-ERK signaling pathway.METHODS: A mouse model of myocardial ischemic reperfusion injury was established.Infarct area, cell apoptosis, and expression of cleaved caspase-3 and phosphorylatied ERK1/2 were determined by TTC/Evans blue staining, TUNEL assay and Western blot, respectively.RESULTS:The mesenchymal characteristics were observed in the EnSCs with expressing CD90 and in absence of CD34 and CD45.EdCC contained (6 811 ±312) ng/g epidermal growth factor (EGF) protein.The phospho-rylation of ERK1/2 markedly increased after injection of EdCC, but was abolished by MEK1 inhibitor PD98059 ( 5 mg/kg) .EdCC decreased the infarct area and apoptotic cell number in the border zone and inhibited caspase-3 activation. However, the effects were abolished by MEK1 specific inhibitor PD98059.EGF did not decrease the infarct area, but the EGF receptor antagonist AG-1487 (6 mg/kg) partly abolished the myocardial protective effect of EdCC.CONCLUSION:EdCC protects the myocardium from ischemic reperfusion injury via activating MEK1-ERK signaling pathway, indicating an essential role in the transmission of stem cell therapy from the cell transplantation to cytokine based strategy.
