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Cell Physiol Biochem. 2017;44(6):2467-2475. doi: 10.1159/000486169. Epub 2017 Dec 18.

Expressions and Regulatory Effects of P38/ERK/JNK Mapks in the Adipogenic Trans-Differentiation of C2C12 Myoblasts.

Qi R1,2, Liu H1, Wang Q1,2, Wang J1, Yang F1,2,3, Long D3, Huang J1,2.

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Chongqing Academy of Animal Science, Rongchang, China.
Key Laboratory of Pig Industry Sciences, Ministry of Agriculture, Rongchang, China.
Chongqing Key Laboratory of Pig Industry Sciences, Rongchang, China.



Myoblasts and muscle satellite cells have the potential to transdifferentiate into adipocytes or adipocyte-like cells. Previous studies suggest that mitogen-activated protein kinase (MAPK) is critical to adipogenic trans-differentiation of muscle cells. ERK1/2, P38 and JNK are three major MAPK family members; their activation and regulatory functions during adipogenic trans-differentiation of myoblasts are investigated.


C2C12 myoblasts were cultured and induced for adipogenic trans-differentiation. Activation patterns of MAPKs were assayed using protein microarray and Western blot. Three specific MAPK blockers, U0126, SB20358 and SP600125, were used to block ERK1/2, P38 and JNK during trans-differentiation. Cellular adipogenesis was measured using staining and morphological observations of cells and expression changes in adipogenic genes.


Inhibitors reduced phosphorylation of corresponding MAPK and produced unique cellular effects. Suppressing P38 promoted adipogenic trans-differentiation and intensified adipolytic metabolism in differentiated cells. However, inhibition of ERK1/2 had the opposite effects on adipogenesis and no effect on adipolysis. Blocking JNK weakly blocked trans-differentiation but stimulated adipolysis and induced apoptosis.


Three MAPKs participate in the regulation of myoblast adipogenic trans-differentiation by controlling adipogenic and adipolysis metabolism.


Adipogenesis; ERK1/2; JNK; MAPK; P38; Trans-differentiation

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