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MAT2A/2B promote porcine intramuscular preadipocyte proliferation through ERK signaling pathway
Author(s) -
Zhao Cunzhen,
Wu Haigang,
Chen Peirong,
Yi Benchi,
Ma Yun,
Deng Kaiwei
Publication year - 2019
Publication title -
animal science journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.606
H-Index - 38
eISSN - 1740-0929
pISSN - 1344-3941
DOI - 10.1111/asj.13264
Subject(s) - cell cycle , microbiology and biotechnology , cyclin d1 , chemistry , gene knockdown , cell growth , mapk/erk pathway , cyclin , signal transduction , flow cytometry , kinase , cyclin b , phosphorylation , cyclin b1 , cyclin d , cell , biology , cyclin dependent kinase 1 , biochemistry , gene
Intramuscular fat (IMF) content has been identified as a crucial factor of porcine meat quality. MAT2A and MAT2B coordinately catalyzes the synthesis of the major biological methyl donor S‐adenosylmethionine (SAMe). However, the regulatory effect of MAT2A and MAT2B on porcine intramuscular preadipocyte proliferation has not been clarified. In this study, we investigated the effect of MAT2A and MAT2B and its potential mechanism during porcine intramuscular proliferation. We demonstrated that overexpression of MAT2A and MAT2B promoted the cell cycle progression of porcine preadipocyte by flow cytometry and EdU‐labeling assay, as well as promoted the expression of cell cycle marker genes including Cyclin B, Cyclin D, and Cyclin‐dependent kinase 4, but reduced the expression of cell cycle inhibitor P27. Consistently, knockdown of MAT2A and MAT2B inhibited cell cycle progression and downregulated the mRNA and protein levels of the above genes. Furthermore, overexpression of MAT2A and MAT2B activated the phosphorylation of ERK1/2. Moreover, the inhibitory effect of U0126 (a specific ERK1/2 inhibitor) on the ERK1/2 activities was partially recovered by overexpression of MAT2A and MAT2B in porcine intramuscular preadipocytes. Taken together, our findings suggested that MAT2A and MAT2B promote porcine preadipocyte proliferation by ERK1/2 signaling pathway.