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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.

Author information

1
Chongqing Academy of Animal Science, Rongchang, China.
2
Key Laboratory of Pig Industry Sciences, Ministry of Agriculture, Rongchang, China.
3
Chongqing Key Laboratory of Pig Industry Sciences, Rongchang, China.

Abstract

BACKGROUND/AIMS:

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.

METHODS:

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.

RESULTS:

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.

CONCLUSION:

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

KEYWORDS:

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

PMID:
29268268
DOI:
10.1159/000486169
[Indexed for MEDLINE]
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