Journal
MOLECULAR ENDOCRINOLOGY
Volume 26, Issue 5, Pages 798-808Publisher
OXFORD UNIV PRESS INC
DOI: 10.1210/me.2011-1287
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Funding
- National Key Basic Research Project [2011CB910201, 2009CB825604]
- National Natural Science Foundation [31030048C120114]
- Shanghai Key Science and Technology Research Project [10JC1401000]
- Program for New Century Excellent Talents in University [NCET-08-0130]
- Shanghai Rising Star Program [08QA14012]
- Shanghai Leading Academic Discipline Project [B110, 985]
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Runx2, a runt-related transcriptional factor family member, is involved in the regulation of osteoblast differentiation. Interestingly, it is abundant in growth-arrested 3T3-L1 preadipocytes and was dramatically down-regulated during adipocyte differentiation. Knockdown of Runx2 expression promoted 3T3-L1 adipocyte differentiation, whereas overexpression inhibited adipocyte differentiation and promoted the trans-differentiation of 3T3-L1 preadipocytes to bone cells. Runx2 was down-regulated specifically by dexamethasone (DEX). Only type I Runx2 was expressed in 3T3-L1 preadipocytes. Using luciferase assay and chromatin immunoprecipitation-quantitative PCR analysis, it was found that DEX repressed this type of Runx2 at the transcriptional level through direct binding of the glucocorticoid receptor (GR) to a GR-binding element in the Runx2 P2 promoter. Further studies indicated that GR recruited histone deacetylase 1 to the Runx2 P2 promoter which then mediated the deacetylation of histone H4 and down-regulated Runx2 expression. Runx2 might play its repressive role through the induction of p27 expression, which blocked 3T3-L1 adipocyte differentiation by inhibiting mitotic clonal expansion. Taken together, we identified Runx2 as a new downstream target of DEX and explored a new pathway between DEX, Runx2, and p27 which contributed to the mechanism of the 3T3-L1 adipocyte differentiation. (Molecular Endocrinology 26: 798-808, 2012)
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