兰尼定受体
细胞生物学
心肌细胞
钙
L型钙通道
MyoD公司
骨骼肌
C2C12型
肌节
钙信号传导
T型钙通道
生物
电压依赖性钙通道
化学
内质网
信号转导
肌发生
内分泌学
有机化学
作者
Tingting Lu,Yifan Zhu,Jiali Guo,Ze-Quan Mo,Quan Zhou,Ching Yuan Hu,Chong Wang
标识
DOI:10.1016/j.bbrc.2023.05.053
摘要
Muscle fiber is the basic unit of skeletal muscle with strong self-adaptability, and its type is closely related to meat quality. Myod family inhibitor (Mdfi) has the function of regulating myogenic regulatory factors during cell differentiation, but how Mdfi regulates muscle fiber type transformation in myoblasts is still unclear. In the present study, we constructed overexpressing and interfering with Mdfi C2C12 cell models by lipofection. The immunofluorescence, quantitative real-time PCR (qPCR), and western blot results show that the elevated MDFI promoted mitochondrial biogenesis, aerobic metabolism and the calcium level by activating CaMKK2 and AMPK phosphorylation and then stimulated the conversion of C2C12 cells from fast glycolytic to slow oxidative type. In addition, after inhibiting IP3R and RYR channels, the higher MDFI reversed the blockage of calcium release from the endoplasmic reticulum by calcium channel receptor inhibitors and increased intracellular calcium levels. Therefore, we propose that the higher MDFI promotes muscle fiber types conversion through the calcium signaling pathway. These findings further broaden our understanding of the regulatory mechanism of MDFI in muscle fiber type transformation. Furthermore, our results suggest potential therapeutic targets for skeletal muscle and metabolic-related diseases.
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