期刊
CELLULAR PHYSIOLOGY AND BIOCHEMISTRY
卷 38, 期 6, 页码 2401-2413出版社
KARGER
DOI: 10.1159/000445592
关键词
Hepatocyte growth factor; Hypoxia; Apoptosis; Autophagy; Cardiomyocyte
资金
- National Natural Science Foundation of China [81441011, 81170102/H0203]
- Priority Academic Program Development of Jiangsu Higher Education Institutions [BL2012011]
- Chinese Medical Association of the Sunlight Foundation [SCRFCMDA201217]
- Collaborative innovation center of Nanjing Medical University
- Fourth Period Project 333 of Jiangsu Province, China [BRA2012207]
Background: Hepatocyte growth factor (HGF) is widely known as a protective factor in ischemic myocardium, however HGF sensitive cellular mechanism remained ill-defined. Autophagy at early stage of hypoxia has been demonstrated to play a role in protecting myocardium both in vivo and vitro. We performed this study to investigate the association between the protective effect of HGF and autophagy. Methods: Ventricular myocytes were isolated from neonatal rat heart (NRVMs). We evaluated cardiomyocytes apoptosis by Hoechst staining and flow cytometry. Autophagy was assessed by transmission electron microscope and mRFP-GFP-LC3 adenovirus infection. Mitochondrial membrane potential was estimated by JC-1 staining. Western blotting and ELISA assay were used to quantify protein concentrations. Results: We found that autophagy in NRVMs increased at early stage after hypoxia and HGF release was consistent with the change of autophagy. Exogenous HGF enhanced autophagy and decreased apoptosis, while neutralizing HGF yielded opposite effects. Besides, inhibition of autophagy increased apoptosis of myocytes. Furthermore, exogenous HGF induced Parkin, the marker of mitochondrial autophagy, indicating increased clearance of injured mitochondria. Conclusions: Our results revealed a potential mechanism in which exogenous HGF prevented NRVMs from apoptosis after hypoxia. Upregulation of Parkin through administration of exogenous HGF may be a potential therapeutic strategy ptotecting myocytes during ischemia. (C) 2016 The Author(s) Published by S. Karger AG, Basel
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