Mstn knockdown decreases the trans-differentiation from myocytes to adipocytes by reducing Jmjd3 expression via the SMAD2/SMAD3 complex |
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Authors: | Li Gao Miaomiao Yang Xueqiao Wang Lei Yang Guangpeng Li |
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Institution: | 1. State Key Laboratory of Reproductive Regulation &2. Breeding of Grassland Livestock, Inner Mongolia University, Hohhot, China |
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Abstract: | ABSTRACTMyostatin (Mstn) is an important growth/differentiation factor, and knockdown of Mstn reduces fat content. Here, we knocked down Mstn expression in C2C12 myoblasts and then induced adipogenic trans-differentiation in the cells. The effects of Mstn knockdown on lipid droplet contents and H3K27me3 marker expression on adipocyte-specific genes were detected. The results showed that Mstn knockdown reduced the formation of lipid droplets, downregulated the expression of adipocyte-specific genes, and increased H3K27me3 marker expression on adipocyte-specific genes. Chromatin immunoprecipitation analysis showed that the SMAD2/SMAD3 complex could combine with the Jumonji D3 (Jmjd3) promoter and that Mstn regulated Jmjd3 expression through this process. Jmjd3 overexpression removed the H3K27me3 marker and increased the expression of adipocyte-specific genes. Overall, our results showed that Mstn regulated Jmjd3 expression through SMAD2/SMAD3, thus affecting the H3K27me3 marker on adipocyte-specific genes and the trans-differentiation from myocytes to adipocytes. |
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Keywords: | Myostatin knockdown adipocyte-specific genes Jumonji D3 SMAD2/SMAD3 H3K27me3 |
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