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TETs are involved in adipogenic differentiation via Hif‐1a mediated regulation of Pparg (817.5)
Author(s) -
Yoo Yeongran,
Park Yoon Jung
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.817.5
Subject(s) - adipogenesis , peroxisome proliferator activated receptor gamma , transcription factor , epigenetics , biology , gene , dna methylation , transcriptional regulation , regulator , regulation of gene expression , cellular differentiation , gene expression , adipocyte , glut4 , microbiology and biotechnology , enhancer , genetics , adipose tissue , peroxisome proliferator activated receptor , biochemistry , chromosomal translocation
TET proteins are a‐Ketoglutarate dependent hydroxylases, which convert 5‐methylcytosine to 5‐hydroxymethylcytosine in DNA. They have been described as key modulators for DNA methylation pattern in locus‐specific and genome‐wide levels. In this study, we showed that the role of TET during 3T3‐L1 cell differentiation in vitro. We found that the Tet1 and Tet2 were induced in 3T3‐L1 cells during adipocyte differentiation, and this pattern paralleled that of other adipogenic gene markers like Pparg and Glut4. RNA‐interference suppression of Tet1 in 3T3‐L1 cells interfered the adipocyte differentiation by downregulating Pparg gene expression, a master regulator for adipoctye specific genes. Furthermore, the depletion of Tet1 led to the elevation of Hif‐1a gene expression, which is a transcription factor for hypoxia regulated genes that has been shown to block adipogenesis by transcriptional inhibition of Pparg. Intriguingly, Hif‐1a has a binding site for both Tet1 and Tet2 in its promoter, suggesting that TETs are possible transcriptional regulators of Hif‐1a. The results demonstrated that TETs, a‐Ketoglutarate‐dependent epigenetic modulator, are involved in adipogenic differentiation via Hif1‐a‐mediated regulation of Pparg. Grant Funding Source : Supported by Korean National Research Foundation of Korea(22A20130012143)