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Heat stress induces apoptosis through disruption of dynamic mitochondrial networks in dairy cow mammary epithelial cells

文献类型： 外文期刊

作者： Chen, Kun-Lin 1 ; Wang, Hui-Li 1 ; Jiang, Lin-Zheng 3 ; Qian, Yong 1 ; Yang, Cai-Xia 4 ; Chang, Wei-Wei 4 ; Zhong, Ji- 1 ;

作者机构： 1.Jiangsu Acad Agr Sci, Jiangsu Key Lab Food Qual & Safety, Minist Sci & Technol, State Key Lab Cultivat Base, Nanjing 210014, Peoples R China

2.Minist Agr, Key Lab Crop & Anim Integrated Farming, Nanjing 210014, Peoples R China

3.Dairy Ind Co Ltd, Youyuan Res Inst, Nanjing 211100, Peoples R China

4.Nanjing Agr Univ, Coll Anim Sci & Technol, Nanjing 210095, Peoples R China

关键词： Heat stress; Mitochondria fission; Mitochondria fusion; Oxidative stress; Dairy cow mammary epithelial cells

期刊名称：IN VITRO CELLULAR & DEVELOPMENTAL BIOLOGY-ANIMAL （ 影响因子：2.416； 五年影响因子：2.117 ）

ISSN： 1071-2690

年卷期： 2020 年 56 卷 4 期

页码：

收录情况： SCI

摘要： Heat stress-induced reductions in milk yield and the dysfunction of mammary glands are economically important challenges that face the dairy industry, especially during summer. The aim of the present study is to investigate the effects of heat stress on mitochondrial function by using dairy cow mammary epithelial cells (DCMECs) as an in vitro model. Live cell imaging shows that the mitochondria continually change shape through fission and fusion. However, heat stress induces the fragmentation of mitochondria, as well as the decreased of ATP level, membrane potential, and anti-oxidant enzyme activity and the increased of respiratory chain complex I activity. In addition, the cytosolic Ca2+ concentration and cytochrome c expression (Cyto-c) were increased after heat stress treatment. Both qRT-PCR and western blot analysis indicate that mitofusin1/2 (Mfn1/2) and optic atrophy protein-1 (Opa-1) are downregulated after heat stress, whereas dynamin-related protein 1 (Drp1) and fission 1 (Fis-1) are upregulated, which explains the observed defect of mitochondrial network dynamics. Accordingly, the present study indicated that heat stress induced the dysfunction of DCMEC through disruption of the normal balance of mitochondrial fission and fusion.

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