| Literature DB >> 30515791 |
Yafan Gong1, Jie Yang1, Jingzeng Cai1, Qi Liu1, Jun Min Zhang2, Ziwei Zhang1,3,4.
Abstract
Glutathione peroxidase 3 (Gpx3), as an important selenoprotein, is the most crucial antioxidant defense in cardiomyocytes. However, the role of Gpx3 in Se-deficient cardiomyocyte damage still less reported. Here, we developed Gpx3 silence cardiomyocytes culture model (small interfering RNA; siRNA) for research the crosstalk between autophagy and apoptosis. Quantitative real-time PCR and western blot analysis are performed to detect the expression of apoptosis and autophagy-related genes. MDC stain, flow cytometry, AO/EB stain, and electron microscope were performed to observe the changes of cell morphology. Our results reveal that Gpx3 suppression can significant increases in ROS (p < 0.05) levels, which further induced apoptosis through upregulated the expression of Caspase-3 in cardiomyocytes. Meanwhile, we also found that the whole process is accompanied by the occurrence of autophagy, which are promoted by inhibiting the mTOR, and increasing the expression of ATG-7, ATG-10, and ATG-12. Altogether, we conclude that the apoptotic and autophagic response machineries share antagonistic function in Gpx3 knockdown cardiomyocytes.Entities:
Keywords: apoptosis; autophagy; cardiomyocytes; chickens; glutathione peroxidase 3
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Year: 2018 PMID: 30515791 DOI: 10.1002/jcp.27842
Source DB: PubMed Journal: J Cell Physiol ISSN: 0021-9541 Impact factor: 6.384