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.

中文翻译：

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热应激通过破坏奶牛乳腺上皮细胞中的动态线粒体网络来诱导凋亡。

热应激引起的牛奶产量下降和乳腺功能障碍是奶业面临的重要经济挑战，特别是在夏季。本研究的目的是通过使用奶牛乳腺上皮细胞（DCMEC）作为体外模型研究热应激对线粒体功能的影响。活细胞成像显示线粒体通过裂变和融合不断改变形状。然而，热应激诱导线粒体破碎，以及ATP水平，膜电位和抗氧化酶活性的降低以及呼吸链复合体I活性的提高。此外，热应激处理后，细胞质中Ca2 +的浓度和细胞色素c的表达（Cyto-c）增加。qRT-PCR和蛋白质印迹分析均表明，热应激后，丝裂霉素1/2（Mfn1 / 2）和视神经萎缩蛋白-1（Opa-1）被下调，而动力相关蛋白1（Drp1）和裂变1（Fis- 1）上调，这解释了观察到的线粒体网络动力学缺陷。因此，本研究表明热应激通过破坏线粒体裂变和融合的正常平衡而引起DCMEC的功能障碍。