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TRIM28 Regulates Dlk1 Expression in Adipogenesis.

Hsin-Pin Lu1, Chieh-Ju Lin1, Wen-Ching Chen1

  • 1Graduate Institute of Biochemical Sciences, College of Life Science, National Taiwan University, Taipei 10617, Taiwan.

International Journal of Molecular Sciences
|October 3, 2020
PubMed
Summary

Tripartite motif-containing protein 28 (TRIM28) is vital for adipogenesis, regulating fat cell differentiation. Its knockdown increases the adipogenesis inhibitor Dlk1, hindering differentiation, but this can be rescued by further Dlk1 knockdown.

Keywords:
DNA methylationDlk1TRIM28adipogenesishistone modification

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Area of Science:

  • Molecular Biology
  • Epigenetics
  • Cell Differentiation

Background:

  • Tripartite motif-containing protein 28 (TRIM28) acts as a transcriptional corepressor, influencing development and differentiation.
  • Adipogenesis, the process of fat cell formation, is a complex regulatory pathway crucial for metabolic homeostasis.

Purpose of the Study:

  • To investigate the role and regulatory mechanisms of TRIM28 in adipogenesis.
  • To identify genes regulated by TRIM28 during the differentiation of 3T3-L1 preadipocytes.

Main Methods:

  • Utilized lentivirus-mediated shRNA to knock down Trim28 expression in 3T3-L1 cells.
  • Performed morphological observation and gene expression analysis to assess differentiation.
  • Employed RNA-sequencing (RNA-seq) to identify TRIM28-regulated genes.
  • Conducted epigenetic analysis, including DNA and histone methylation assays on the Dlk1 promoter.

Main Results:

  • TRIM28 knockdown significantly impaired 3T3-L1 preadipocyte differentiation.
  • RNA-seq revealed increased expression of delta-like homolog 1 (Dlk1), an adipogenesis inhibitor, in TRIM28-knockdown cells.
  • Knockdown of Dlk1 rescued the impaired differentiation observed in TRIM28-knockdown cells.
  • Epigenetic analysis showed altered histone methylation (increased H3K4, decreased H3K27) at the Dlk1 promoter, but not DNA methylation changes.
  • TRIM28 may be recruited by transcription factor E2f1 to regulate Dlk1 expression.

Conclusions:

  • The TRIM28-Dlk1 axis plays a critical role in regulating adipogenesis.
  • TRIM28 influences adipocyte differentiation potentially through epigenetic modulation of key genes like Dlk1.
  • Understanding this pathway offers insights into metabolic regulation and potential therapeutic targets.