Exogenous hydrogen sulfide enhances myogenic differentiation of C2C12 myoblasts under high palmitate stress

Skeletal muscle atrophy was one of main complications of type 2 diabetes mellitus. Hydrogen sulfide (H2S) is involved in various physiological functions, such as anti-hypertension and anti-oxidant. Skeletal muscle atrophy caused by type 2 diabetes could lead to the regeneration of muscle fibers. Wnt...

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Published inHeliyon Vol. 10; no. 19; p. e38661
Main Authors Lu, Fangping, Zhang, Shiwu, Dong, Shiyun, Wang, Mengyi, Pang, Kemiao, Zhao, Yajun, Huang, Jiayi, Kang, Jiaxin, Liu, Ning, Zhang, Xueya, Zhao, Dechao, Lu, Fanghao, Zhang, Weihua
Format Journal Article
LanguageEnglish
Published Elsevier Ltd 01.10.2024
Elsevier
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Summary:Skeletal muscle atrophy was one of main complications of type 2 diabetes mellitus. Hydrogen sulfide (H2S) is involved in various physiological functions, such as anti-hypertension and anti-oxidant. Skeletal muscle atrophy caused by type 2 diabetes could lead to the regeneration of muscle fibers. Wnt signaling pathway plays a crucial important role in this process. H2S maybe regulate the Wnt signaling pathway to alleviate skeletal muscle atrophy, however, this role has not been clarified. The aim of this study is to investigate the potential regulatory role of H2S in the Wnt signaling pathway. C2C12 myoblasts treated with 500 μmol palmitate as an in vitro model. Western blot was used to detect the levels of CSE, PKM1, β-catenin, MuRF1, MYOG, MYF6 and MYOD1. In addition, MuRF1 was mutated at Cys44 and MuRF1 S-sulfhydration was detected by biotin switch assay. The interaction between PKM1 and MuRF1 was assessed via Co-immunoprecipitation. Differentiation of C2C12 myoblasts was evaluated using LAMININ staining. These data showed the levels of CSE, β-catenin, PKM1, MYOG, MYF6 and MYOD1 were decreased in pal group, compared with control and pal + NaHS groups. MuRF1 Cys44 mutants increased the protein levels of β-catenin, MYOG, MYF6 and MYOD1 in pal group. Our results suggest that H2S regulates the S-sulfhydration levels of MuRF1 at Cys44, influencing the ubiquitination levels of PKM1 and ultimately promoting myoblast differentiation. •Hydrogen sulfide (H2S) mitigates skeletal muscle atrophy in type 2 diabetes via Wnt signaling pathway.•MuRF1 mutation at Cys44 enhances β-catenin, MYOG, MYF6, and MYOD1 protein levels.•H2S regulates MuRF1 S-sulfhydration at Cys44, impacting PKM1 ubiquitination.•H2S promotes myoblast differentiation, offering insights into diabetic muscle atrophy.
ISSN:2405-8440
2405-8440
DOI:10.1016/j.heliyon.2024.e38661