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UFBP1 Ameliorates Heat Stress-Induced Apoptosis via Mitochondria-Mediated Pathway in Bovine Mammary Epithelial Cells

文献类型： 外文期刊

作者： Li, Yuan 1 ; Yu, Ran 1 ; Tan, Shujing 1 ; Jiang, Yunlong 1 ; Sun, Longwei 1 ; Shen, Manman 1 ; Zhang, Chuanjian 3 ; Chen, Kunlin 4 ; Li, Chengmin 1 ;

作者机构： 1.Jiangsu Univ Sci & Technol, Sch Biotechnol, Jiangsu Key Lab Sericultural & Anim Biotechnol, Zhenjiang 212100, Peoples R China

2.Chinese Acad Agr Sci, Sericultural Res Inst, Key Lab Silkworm & Mulberry Genet Improvement, Minist Agr & Rural Affairs, Zhenjiang 212100, Peoples R China

3.Jiangsu Acad Agr Sci, Inst Vet Immunol & Engn, Nanjing 210014, Peoples R China

4.Jiangsu Acad Agr Sci, Inst Anim Sci, Minist Agr & Rural Affairs, Nanjing 210014, Peoples R China

关键词： heat stress; bovine mammary epithelial cells (BMECs); UFBP1; mitochondrial function; apoptosis; milk synthesis

期刊名称：ANIMALS （ 影响因子：2.7； 五年影响因子：3.2 ）

ISSN： 2076-2615

年卷期： 2025 年 15 卷 9 期

页码：

收录情况： SCI

摘要： Heat stress in dairy cows is aggravated by Global warming, which negatively affects their performance and health, especially high yielding cows are more susceptible to high temperature and humidity in summer. Besides increasing body temperature and reducing feed intake, heat stress also compromises mammary gland function by inducing apoptosis in bovine mammary epithelial cells (BMECs). UFBP1 (Ufm1-binding protein 1) serves as an essential component of ufmylation, is crucial for the preservation of cellular homeostasis. However, little is known about its contribution to heat stress-induced apoptosis in BMECs. Therefore, the present study aimed to elucidate the effect of UFBP1 on heat stress-induced apoptosis through knockdown and overexpression of UFBP1 in BMECs. The results showed that heat stress triggered cell apoptosis (increased apoptosis rate and Bax/Bcl-2 protein expression) and decreased the expression of genes associated with the production of milk fat and protein both in vivo and in vitro studies. Furthermore, UFBP1 silencing aggravated the high-temperature-induced cell damage, and overexpression of UFBP1 attenuated heat stress-induced mitochondrial dysfunction, as evidenced by increased mitochondrial membrane potential (MMP), ATP synthesis and NAD+/NADH ratio, as well as the reduced reactive oxygen species (ROS) generation. Importantly, the mitochondrial apoptosis pathway triggered by heat stress was blocked by UFBP1, as indicated by the reduced apoptosis rate and Bax/Bcl-2 protein expression. In addition, UFBP1 restored the expression of milk fat and protein-related genes in heat-stressed BMECs. In conclusion, these findings indicate that UFBP1 may serve as a promising therapeutic target for ameliorating heat stress in dairy cows, thereby providing novel theoretical insights into the mitigation of adverse thermal stress effects on livestock productivity.

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