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Mitsugumin 53 promotes mitochondrial autophagy through regulating Ambra1 expression in C2C12 myoblast cells
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AbstractIn this study, we investigated the function of Mitsugumin 53 (MG53) in regulation of mitochondrial autophagy in skeletal muscle cells and explored its potential application in the prevention and treatment of skeletal muscle atrophy in rats with chronic kidney disease (CKD). The expression of autophagy beclin 1 regulator 1 (Ambra1) and MG53 in skeletal muscles of 5/6 nephrectomized rats was measured, and the effect of MG53 on mitochondrial autophagy of C2C12 myoblasts was investigated by in vitro experiments. Our results show the expression of Ambra1 and MG53 in the skeletal muscle of CKD rats was significantly decreased. In vitro experiments showed that MG53 overexpression could promote the expression of Ambra1 and mitochondrial autophagy in C2C12 cells, suggesting that recovery of autophagy by MG53 intervention may help remove abnormal mitochondria and alleviate muscle atrophy. In conclusion, the damaged or functionally incomplete mitochondria in CKD rats could not be effectively removed, which may be related to the low activity of Ambra1. In vitro experiments showed that MG53 overexpression could promote the expression of Ambra1 in C2C12 cells and restore mitochondrial autophagy. Whether MG53 can help remove abnormal mitochondria and relieve CKD‐induced muscle atrophy requires further study.
Title: Mitsugumin 53 promotes mitochondrial autophagy through regulating Ambra1 expression in C2C12 myoblast cells
Description:
AbstractIn this study, we investigated the function of Mitsugumin 53 (MG53) in regulation of mitochondrial autophagy in skeletal muscle cells and explored its potential application in the prevention and treatment of skeletal muscle atrophy in rats with chronic kidney disease (CKD).
The expression of autophagy beclin 1 regulator 1 (Ambra1) and MG53 in skeletal muscles of 5/6 nephrectomized rats was measured, and the effect of MG53 on mitochondrial autophagy of C2C12 myoblasts was investigated by in vitro experiments.
Our results show the expression of Ambra1 and MG53 in the skeletal muscle of CKD rats was significantly decreased.
In vitro experiments showed that MG53 overexpression could promote the expression of Ambra1 and mitochondrial autophagy in C2C12 cells, suggesting that recovery of autophagy by MG53 intervention may help remove abnormal mitochondria and alleviate muscle atrophy.
In conclusion, the damaged or functionally incomplete mitochondria in CKD rats could not be effectively removed, which may be related to the low activity of Ambra1.
In vitro experiments showed that MG53 overexpression could promote the expression of Ambra1 in C2C12 cells and restore mitochondrial autophagy.
Whether MG53 can help remove abnormal mitochondria and relieve CKD‐induced muscle atrophy requires further study.
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