Journal
CELL AND TISSUE RESEARCH
Volume 354, Issue 3, Pages 761-770Publisher
SPRINGER
DOI: 10.1007/s00441-013-1696-5
Keywords
Axin2; Wnt/beta-catenin; Mesenchymal progenitor cells; Adipocyte; Differentiation
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Funding
- dental research center, Nihon University School of Dentistry
- Sato Fund, Nihon University School of Dentistry
- Ministry of Education, Culture, Sports, Science and Technology of Japan [21791799]
- Grants-in-Aid for Scientific Research [21791799] Funding Source: KAKEN
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Dexamethasone (Dex) regulates osteoblastic and adipocytic differentiation in mesenchymal progenitor cells through regulation of Wnt/beta-catenin signaling. To elucidate the regulatory mechanisms underlying the effects of Dex, we examine the expression of Axin2, which is an intracellular inhibitor of Wnt/beta-catenin signaling, in ROB-C26 clonal mesenchymal progenitor cells (C26). We observed the induction of Axin2 mRNA in C26 cells in response to Dex treatment. Treatment with a glucocorticoid receptor (GR) antagonist, mifepristone, showed that Dex-induced up-regulation of Axin2 is mediated by the GR. In the absence of Dex, gene silencing by using Axin2-targeted short hairpin RNA increased the number of alkaline phosphatase (ALP)-positive and nuclear beta-catenin-positive cells and ALP activity. In the presence of Dex, Axin2 knockdown resulted in an increased number of ALP-positive and nuclear beta-catenin-positive cells. Furthermore, Axin2 knockdown in Dex-treated cells suppressed adipocyte differentiation (as determined by reduced Oil Red O staining), reduced the number of PPAR gamma-positive and aP2-positive cells and decreased the mRNA expression of PPAR gamma 2 and aP2. These results suggest that Axin2 plays a key role in adipocyte and osteoblastic differentiation by controlling beta-catenin expression.
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