miR-27a-3p relieves heat stress-induced mitochondrial damage and aberrant milk protein synthesis through MEK/ERK pathway in BMECs

文献类型： 外文期刊

第一作者： Wang, Yue

作者： Wang, Yue;Xia, Shu-Wen;Zhao, Fang;Ding, Qiang;Ye, Xiao-Mei;Zhong, Ji-Feng;Chen, Kun-Lin;Wang, Hui-Li;Wang, Yue;Xia, Shu-Wen;Zhao, Fang;Ding, Qiang;Ye, Xiao-Mei;Zhong, Ji-Feng;Chen, Kun-Lin;Wang, Hui-Li;Wu, Jie

作者机构：

关键词： miR-27a-3p; Mitochondrial damage; Cell proliferation; Lactation; MEK; ERK signaling pathway

期刊名称：CELL STRESS & CHAPERONES （ 影响因子：3.8； 五年影响因子：3.7 ）

ISSN： 1355-8145

年卷期： 2023 年

页码：

收录情况： SCI

摘要： With global warming, heat stress has become a primary factor that compromises the health and milk quality of dairy cows. Here, we investigated the function and underlying regulatory mechanism of miR-27a-3p in bovine mammary epithelial cells (BMECs) under heat-stress conditions. The current study showed that miR-27a-3p could prevent heat stress-induced BMEC oxidative stress and mitochondrial damage by regulating the balance between mitochondrial fission and fusion processes. Importantly, we found that miR-27a-3p could increase cell proliferation under heat stress conditions by regulating the MEK/ERK pathway and cyclin D1/E1. Interestingly, miR-27a-3p is also involved in the regulation of milk protein synthesis-related protein expression, such as CSN2 and ELF5. Inhibition of the MEK/ERK signaling pathway by AZD6244 blocked the regulatory function of miR-27a-3p in cell proliferation and milk protein synthesis in BMECs under heat stress conditions. Our findings demonstrated that miR-27a-3p protects BMECs from heat stress-induced oxidative stress and mitochondrial damage through the MEK/ERK pathway, thereby promoting BMECs proliferation and lactation in dairy cows.

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