5mC profiling characterized TET2 as an anti-adipogenic demethylase

Gene. 2020 Apr 5:733:144265. doi: 10.1016/j.gene.2019.144265. Epub 2019 Dec 2.

Abstract

To explore its roles in adipogenesis, the levels of genomic 5mC methylation were examined across the adipocyte differentiation of 3 T3-L1 cells. This led to the identification of an up-regulating 5mC profile during the process. To further explore the regulation, gene expression assay was performed with a set of 5mC metabolic enzymes. Among them, TET2 was found to be the most regulated 5mC demethylase, in addition to a well-investigated 5mC methylase DNMT1. In the process, the expression of Tet2 increased for over 16-fold, suggesting its implications in the differentiation. Therefore, loss-of-function and gain-of-function assays were performed with Tet2. It was found that in relative to the differentiation of wild-type cells, knockdown of Tet2 expression led to greatly enhanced differentiation process, while over-expression of the gene resulted in repressed differentiation. Pathway study found that during the differentiation, TET2 demethylates Adrb3 promoter to up-regulate its expression. This led to enhanced lipolysis and decreased lipid production. To the upstream pathway, vitamin C treatment was found to enhance the activity of TETs, decrease 5mC levels and repress lipid production. Taken together, TET2 was characterized as an anti-adipogenic demethylase in adipocyte differentiation of 3 T3-L1 cells.

Keywords: Adipogenesis; DNA methylation; Lipolysis; TET2.

MeSH terms

  • 3T3-L1 Cells
  • 5-Methylcytosine / metabolism
  • Adipocytes / metabolism
  • Adipogenesis / genetics
  • Adipogenesis / physiology
  • Animals
  • Cell Differentiation / genetics
  • DNA Methylation*
  • DNA-Binding Proteins / genetics
  • DNA-Binding Proteins / metabolism*
  • Dioxygenases
  • Epigenesis, Genetic
  • Gene Expression / genetics
  • Lipolysis / genetics
  • Mice
  • Promoter Regions, Genetic
  • Proto-Oncogene Proteins / genetics
  • Proto-Oncogene Proteins / metabolism*
  • Receptors, Adrenergic, beta-3 / genetics
  • Receptors, Adrenergic, beta-3 / metabolism
  • Transcription Factors / genetics

Substances

  • Adrb3 protein, mouse
  • DNA-Binding Proteins
  • Proto-Oncogene Proteins
  • Receptors, Adrenergic, beta-3
  • Transcription Factors
  • 5-Methylcytosine
  • Dioxygenases
  • Tet2 protein, mouse