4.5 Article

Differentiated embryo chondrocyte 1 (DEC1) represses PPARγ2 gene through interacting with CCAAT/enhancer binding protein β (C/EBPβ)

Journal

MOLECULES AND CELLS
Volume 33, Issue 6, Pages 575-581

Publisher

KOREAN SOC MOLECULAR & CELLULAR BIOLOGY
DOI: 10.1007/s10059-012-0002-9

Keywords

adipogenesis; C/EBP beta; DEC1; hypoxia; PPAR gamma

Funding

  1. Korea Healthcare technology RD Project [A090616]
  2. Korea Health Promotion Institute [A090616] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
  3. National Research Foundation of Korea [핵06A3102] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

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DEC1 is a transcription repressor that is induced by Hypoxia-Inducible Factor-alpha/beta (HIF-alpha/beta). In this study, we found that either hypoxic treatment or ectopic expression of DEC1 blocks induction of a master adipogenic transactivator, peroxisome proliferative activated receptor-gamma 2 (PPAR gamma 2) in 3T3-L1 cells. DEC1 did not prevent C/EBP beta, which is an upstream transactivator for PPAR gamma 2, from occupying the PPAR gamma 2 promoter. DEC1 occupied the PPAR gamma 2 promoter by interacting with DNA-bound C/EBP beta. DEC1 occupancy was accompanied by a reduction of acetylated histones and an increase in histone deacetylase 1 (HDAC1) occupancy on the PPAR gamma 2 promoter. Based on the fact that DEC1 interacts with HDAC1, this study suggests that DEC1 blocks adipogenesis by reinforcing HDAC1 recruitment to the PPAR gamma 2 promoter. This study implies that DEC1 is one of the mediators that reset the pattern of PPAR gamma 2 expression in response to hypoxia.

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