Serum regulates adipogenesis of mesenchymal stem cells via MEK/ERK‐dependent PPARγ expression and phosphorylation

Mesenchymal stem cells (MSCs) provide us an excellent cellular model to uncover the molecular mechanisms underlying adipogenic differentiation of adult stem cells. PPARγ had been considered as an important molecular marker of cells undergoing adipogenic differentiation. Here, we demonstrated that ex...

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Bibliographic Details
Published in:Journal of cellular and molecular medicine 2010-04, Vol.14 (4), p.922-932
Main Authors: Wu, Ling, Cai, Xiaoxiao, Dong, Hai, Jing, Wei, Huang, Yuanding, Yang, Xingmei, Wu, Yao, Lin, Yunfeng
Format: Article
Language:English
Subjects:
Adipocytes
Adipogenesis
Body fat
Bone marrow
Cell culture
Cell differentiation
Dexamethasone
extracellular signal‐regulated kinase
Gene expression
Indomethacin
Insulin resistance
Kinases
Ligands
Mesenchymal stem cells
mitogen‐activated protein kinase
Molecular modelling
Peroxisome proliferator-activated receptors
peroxisome proliferator–activated receptor γ
Phosphorylation
Proteins
Signal transduction
Stem cells
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Summary:Mesenchymal stem cells (MSCs) provide us an excellent cellular model to uncover the molecular mechanisms underlying adipogenic differentiation of adult stem cells. PPARγ had been considered as an important molecular marker of cells undergoing adipogenic differentiation. Here, we demonstrated that expression and phosphorylation of PPARγ could be found in bone marrow–derived MSCs cultured in expansion medium without any adipogenic additives (dexamethasone, IBMX, insulin or indomethacin). Then, PPARγ was dephosphorylated in MSCs during the process of adipogenic differentiation. We then found that inhibition of MEK activation by specific inhibitor (PD98059) counteracted the PPARγ expression and phosphorylation. However, expression and phosphorylation of PPARγ did not present in MSCs cultured in medium with lower serum concentration. When these MSCs differentiated into adipocytes, no phosphorylation could be detected to accompany the expression of PPARγ. Moreover, exposure of MSCs to higher concentration of serum induced stronger PPARγ expression, and subsequently enhanced their adipogenesis. These data suggested that activation of the MEK/ERK signalling pathway by high serum concentration promoted PPARγ expression and phosphorylation, and subsequently enhanced adipogenic differentiation of MSCs.
ISSN:1582-1838
1582-4934
DOI:10.1111/j.1582-4934.2009.00709.x