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Research Project: Improving Dairy Cow Feed Efficiency and Environmental Sustainability Using Genomics and Novel Technologies to Identify Physiological Contributions and Adaptations

Location: Animal Genomics and Improvement Laboratory

Title: Sodium butyrate induces mitophagy and apoptosis of bovine skeletal muscle satellite cells through the mammalian target of rapamycin signaling pathway

item DING, YANLING - Ningxia University
item WANG, PENGFEI - Ningxia University
item ZHANG, YANGFENG - Ningxia University
item YANG, CHAOYUN - Ningxia University
item ZHOU, XIAONAN - Ningxia University
item WANG, XIAOWEI - Ningxia University
item LI, CHENGLONG - Ningxia University
item SU, ZUNHUA - Ningxia University
item MING, WENXUAN - Ningxia University
item ZENG, LING - Ningxia University
item SHI, YUANGANG - Ningxia University
item Li, Congjun - Cj
item KANG, XIAOLONG - Ningxia University

Submitted to: International Journal of Molecular Sciences
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 8/28/2023
Publication Date: 8/30/2023
Citation: Ding, Y., Wang, P., Zhang, Y., Yang, C., Zhou, X., Wang, X., Li, C., Su, Z., Ming, W., Zeng, L., Shi, Y., Li, C., Kang, X. 2023. Sodium butyrate induces mitophagy and apoptosis of bovine skeletal muscle satellite cells through the mammalian target of rapamycin signaling pathway. International Journal of Molecular Sciences. 24:13474.

Interpretive Summary: Present study results demonstrated that sodium butyrate subdued the proliferation and increased apoptosis in bovine skeletal muscle satellite cells. Further, sodium butyrate treatment significantly promoted mitophagy and ROS response and decreased the mitochondrial membrane potential. It was also shown that sodium butyrate might regulate apoptosis and mitophagy in bovine skeletal muscle satellite cells by downregulating the mTOR signaling pathway. The present results indicated that sodium butyrate may be a critical metabolic molecule in muscle development, energy metabolism, and regulation of mitochondrial function.

Technical Abstract: Sodium butyrate (NaB) is one of the short-chain fatty acids and is notably produced in large amounts from dietary fiber in the gut. Recent evidence suggests that NaB induces cell proliferation and apoptosis. The skeletal muscle is rich in plenty of mitochondrial. However, it is unclear how NaB acts on host muscle cells and whether it is involved in mitochondria-related functions in myocytes. The present study aimed to investigate the role of NaB treatment on the proliferation, apoptosis, and mitophagy of bovine skeletal muscle satellite cells (BSCs). The results showed that NaB inhibited the proliferation and promoted apoptosis of BSCs and promoted mitophagy in a time and dose-dependent manner in BSCs. In addition, 1mM NaB increased the mitochondrial ROS level, decreased the mitochondrial membrane potential (MMP), increased the number of autophagic vesicles in mitochondria, and increased the mitochondrial DNA (mtDNA) and ATP level. The effects of the mTOR pathway on BSCs were investigated, and the results showed that 1mM NaB inhibited the mRNA and protein expression of mTOR and genes AKT1, FOXO1, and EIF4EBP1 in the mTOR signaling pathway, while the addition of PP242, an inhibitor of the mTOR signaling pathway, also inhibited mRNA and protein expression levels of mTOR, AKT1, FOXO1, and EIF4EBP1, and promoted mitophagy and apoptosis, which were consistent with the effect of NaB treatment. In conclusion, NaB might promote mitophagy and apoptosis in BSCs by inhibiting the mTOR signaling pathway. Our results would expand the knowledge of sodium butyrate on bovine skeletal muscle cell state and mitochondrial function.