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Role of mitochondrial dysfunction and PINK1/Parkin-mediated mitophagy in Cd-induced hepatic lipid accumulation in chicken embryos

文献类型： 外文期刊

作者： Chen, Dawei 1 ; Di Ran 1 ; Wang, Chao 1 ; Liu, Yinyin 1 ; Ma, Yonggang 1 ; Song, Ruilong 1 ; Gao, Yushi 1 ; Liu, Zongping 1 ;

作者机构： 1.Yangzhou Univ, Jiangsu Coinnovat Ctr Prevent & Control Important, Yangzhou 225009, Jiangsu, Peoples R China

2.Yangzhou Univ, Coll Vet Med, Yangzhou 225009, Jiangsu, Peoples R China

3.Chinese Acad Agr Sci, Poultry Inst, Yangzhou 225125, Jiangsu, Peoples R China

4.Yangzhou Univ, Minist Educ China, Joint Int Res Lab Agr & Agriprod Safety, Yangzhou 225009, Jiangsu, Peoples R China

关键词： Chicken; Liver; Hepatocyte; Lipid metabolism; Cadmium; Mitophagy; PINK1; Parkin

期刊名称：LIFE SCIENCES （ 影响因子：5.037； 五年影响因子：4.69 ）

ISSN： 0024-3205

年卷期： 2021 年 284 卷

页码：

收录情况： SCI

摘要： The present study was performed to investigate the effects of Cd exposure on lipid metabolism and mitochondrial dysfunction and to explore the role of mitophagy in Cd-induced dysregulation of lipid metabolism in chicken embryo liver tissues and hepatocytes. To this end, seven-day-old chicken embryos were exposed to different concentrations of Cd for 7 days, and primary chicken embryo hepatocytes were treated with Cd at four different concentrations for 6 h. Furthermore, the mitophagy inhibitor cyclosporine A (CsA) was used to investigate the role of mitophagy in Cd-induced disruption of lipid metabolism. Lipid accumulation, the expression levels of genes involved in lipid metabolism, mitochondrial dysfunction, and mitophagy were measured. The results demonstrated that Cd exposure increases hepatic triglyceride (TG) accumulation and the expression levels of lipogenic genes while decreasing those of lipolytic genes. Furthermore, Cd exposure was observed to alter mitochondrial morphology in terms of reduced size, excessive mitochondrial damage, and the formation of mitophagosomes. The co-localization of lysosome-associated membrane glycoprotein 2 and LC3 puncta was significantly increased in primary chicken embryo hepatocytes after Cd exposure. Moreover, Cd exposure increased LC3, PINK1, and Parkin protein expression levels. CsA effectively alleviated Cd-induced mitochondrial dysfunction, blocked mitochondrial membrane potential collapse, and suppressed PINK1/Parkin-mediated mitophagy. Furthermore, CsA treatment reversed the Cd-induced TG accumulation in liver tissues but further increased it in hepatocytes. Taken together, our findings demonstrate (for the first time) the importance of mitochondrial dysfunction and mitophagy via the PINK1/Parkin pathway in Cd-induced disruption of lipid metabolism.

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