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Effect of Gpx3 gene silencing by siRNA on apoptosis and autophagy in chicken cardiomyocytes
Author(s) -
Gong Yafan,
Yang Jie,
Cai Jingzeng,
Liu Qi,
Zhang Jun min,
Zhang Ziwei
Publication year - 2019
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.27842
Subject(s) - autophagy , gene knockdown , microbiology and biotechnology , apoptosis , gene silencing , small interfering rna , atg5 , gpx3 , biology , chemistry , transfection , cell culture , glutathione peroxidase , glutathione , gene , biochemistry , genetics , enzyme
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.