IGF-II-mediated downregulation of peroxisome proliferator-activated receptor-γ coactivator-1α in myoblast cells involves PI3K/Akt/FoxO1 signaling pathway View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2017-04-03

AUTHORS

Xiaoyu Mu, Weihong Qi, Yunzhang Liu, Jianfeng Zhou, Yun Li, Xiaozhi Rong, Ling Lu

ABSTRACT

Insulin-like growth factor II (IGF-II) can stimulate myogenesis and is critically involved in skeletal muscle differentiation. The presence of negative regulators of this process, however, is not well explored. Here, we showed that in myoblast cells, IGF-II negatively regulated peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) mRNA expression, while constitutive expression of PGC-1α induced myoblast differentiation. These results suggest that the negative regulation of PGC-1α by IGF-II may act as a negative feedback mechanism in IGF-II-induced myogenic differentiation. Reporter assays demonstrated that IGF-II suppresses the basal PGC-1α promoter activity. Blocking the IGF-II signaling pathway increased the endogenous PGC-1α levels. In addition, pharmacological inhibition of PI3 kinase activity prevented the downregulation of PGC-1α but the activation of mTOR was not required for this process. Importantly, further analysis showed that forkhead transcription factor FoxO1 contributes to mediating the effects of IGF-II on PGC-1 promoter activity. These findings indicate that IGF-II reduces PGC-1α expression in skeletal muscle cells through a mechanism involving PI3K–Akt–FoxO1 but not p38 MAPK or Erk1/2 MAPK pathways. More... »

PAGES

199-208

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s11010-017-3010-4

DOI

http://dx.doi.org/10.1007/s11010-017-3010-4

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1084510815

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/28374141


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