AUTHOR=Lu Jiawei , Li Huixia , Yu Debing , Zhao Peng , Liu Yuan 

TITLE=Heat stress inhibits the proliferation and differentiation of myoblasts and is associated with damage to mitochondria

JOURNAL=Frontiers in Cell and Developmental Biology

VOLUME=11

YEAR=2023

URL=https://www.frontiersin.org/journals/cell-and-developmental-biology/articles/10.3389/fcell.2023.1171506

DOI=10.3389/fcell.2023.1171506

ISSN=2296-634X

ABSTRACT=<p><bold>Introduction:</bold> Heat stress is harmful to the health of humans and animals, more and more common, as a consequence of global warming, while the mechanism that heat stress modulates skeletal development remains unknown. Hence, we conducted a model of heat stress <italic>in vitro</italic>.</p><p><bold>Methods:</bold> We used Hu sheep myoblasts as the research object, real-time quantitative PCR (RT-qPCR) and western blot (WB) were conducted to detect the expression of mRNA and protein in heat-stressed myoblasts. The would-healing assay was used to detect the migration of myoblasts. The mitochondria were observed by a transmission electron microscope.</p><p><bold>Results:</bold> mRNA and protein expression of HSP60 was significantly enriched in the heat-stressed myoblasts during proliferation and differentiation (<italic>p</italic> &lt; 0.05). In our study, we indicated that heat stress enriched the intracellular ROS of the myoblasts (<italic>p</italic> &lt; 0.001), leading to an increase in autophagy in the myoblasts to induce apoptosis. The results demonstrated that the protein expression of LC3B-1 and BCL-2 was significantly increased in myoblasts under heat stress during proliferation and differentiation (<italic>p</italic> &lt; 0.05). Additionally, heat stress inhibited mitochondrial biogenesis and function and reduced the mitochondrial membrane potential and downregulated the expression of <italic>mtCo2, mtNd1</italic> and <italic>DNM1L</italic> (<italic>p</italic> &lt; 0.05) in myoblasts during proliferation and differentiation. Consequently, heat stress inhibited the proliferation and differentiation of the myoblasts, in accordance with the downregulation of the expression of <italic>PAX7, MYOD, MYF5, MYOG</italic> and <italic>MYHC</italic> (<italic>p</italic> &lt; 0.05). Moreover, heat stress also inhibited the cell migration of the myoblasts.</p><p><bold>Discussion:</bold> This work demonstrates that heat stress inhibits proliferation and differentiation, and accelerates apoptosis by impairing mitochondrial function and promoting autophagy, which provides a mechanism to understand heat stress affects the development of the skeletal muscle.</p>