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Mol. Cells 2012; 33(6): 575-581

Published online May 18, 2012

https://doi.org/10.1007/s10059-012-0002-9

© The Korean Society for Molecular and Cellular Biology

Differentiated Embryo Chondrocyte 1 (DEC1) Represses PPARγ2 Gene through Interacting with CCAAT/Enhancer Binding Protein β(C/EBPβ)

Young-Kwon Park, and Hyunsung Park*

Department of Life Science, University of Seoul, Seoul 130-743, Korea

Correspondence to : *Correspondence: hspark@uos.ac.kr

Received: January 3, 2012; Revised: March 20, 2012; Accepted: March 28, 2012

Abstract

DEC1 is a transcription repressor that is induced by Hy-poxia-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-gamma2 (PPAR gamma 2) in 3T3-L1 cells. DEC1 did not prevent C/EBP beta, which is an upstream transactivator for PPAR gamma 2, from occupy-ing the PPARgamma2 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.

Keywords adipogenesis, C/EBP beta, DEC1, hypoxia, PPAR gamma

Article

Research Article

Mol. Cells 2012; 33(6): 575-581

Published online June 30, 2012 https://doi.org/10.1007/s10059-012-0002-9

Copyright © The Korean Society for Molecular and Cellular Biology.

Differentiated Embryo Chondrocyte 1 (DEC1) Represses PPARγ2 Gene through Interacting with CCAAT/Enhancer Binding Protein β(C/EBPβ)

Young-Kwon Park, and Hyunsung Park*

Department of Life Science, University of Seoul, Seoul 130-743, Korea

Correspondence to:*Correspondence: hspark@uos.ac.kr

Received: January 3, 2012; Revised: March 20, 2012; Accepted: March 28, 2012

Abstract

DEC1 is a transcription repressor that is induced by Hy-poxia-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-gamma2 (PPAR gamma 2) in 3T3-L1 cells. DEC1 did not prevent C/EBP beta, which is an upstream transactivator for PPAR gamma 2, from occupy-ing the PPARgamma2 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.

Keywords: adipogenesis, C/EBP beta, DEC1, hypoxia, PPAR gamma

Mol. Cells
Sep 30, 2023 Vol.46 No.9, pp. 527~572
COVER PICTURE
Chronic obstructive pulmonary disease (COPD) is marked by airspace enlargement (emphysema) and small airway fibrosis, leading to airflow obstruction and eventual respiratory failure. Shown is a microphotograph of hematoxylin and eosin (H&E)-stained histological sections of the enlarged alveoli as an indicator of emphysema. Piao et al. (pp. 558-572) demonstrate that recombinant human hyaluronan and proteoglycan link protein 1 (rhHAPLN1) significantly reduces the extended airspaces of the emphysematous alveoli by increasing the levels of TGF-β receptor I and SIRT1/6, as a previously unrecognized mechanism in human alveolar epithelial cells, and consequently mitigates COPD.

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