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- Title
miR-27a-3p relieves heat stress-induced mitochondrial damage and aberrant milk protein synthesis through MEK/ERK pathway in BMECs.
- Authors
Wang, Yue; Wu, Jie; Xia, Shu-Wen; Zhao, Fang; Ding, Qiang; Ye, Xiao-Mei; Zhong, Ji-Feng; Chen, Kun-Lin; Wang, Hui-Li
- Abstract
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. The potential regulatory mechanism of miR-27a-3p in attenuating heat stress-induced apoptosis and lactation defect in BMECs.
- Subjects
MILK proteins; PHYSIOLOGICAL effects of heat; PROTEIN synthesis; MITOCHONDRIA; CELL physiology; DAIRY cattle
- Publication
Cell Stress & Chaperones, 2023, Vol 28, Issue 3, p265
- ISSN
1355-8145
- Publication type
Article
- DOI
10.1007/s12192-023-01334-z