Association Between Proteasome 26S Subunit, Non-ATPase 3 Methylation and Insulin β Cell Apoptosis in Type 2 Diabetic

Guiping Huang1,2, Guodong He1,2, Shaoxian Chen1

  • 1Medical Research Institute, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, People's Republic of China.

Abstract

Insights

Methylation of PSMD3 (proteasome subunit 3) is upregulated in type 2 diabetes mellitus (T2DM) and may influence cell apoptosis and proliferation by affecting USP14 activity. This research explores PSMD3 methylation

Area of Science:

  • Molecular Biology
  • Biochemistry
  • Genetics

Background:

  • The role of PSMD3 methylation in type 2 diabetes mellitus (T2DM) pathogenesis is not fully understood.
  • PSMD3 methylation's impact on protein stability and degradation may be significant in T2DM development.

Purpose of the Study:

  • To investigate the molecular and bioinformatic characteristics of PSMD3 methylation in T2DM.
  • To explore the association between PSMD3 methylation and T2DM pathogenesis.

Main Methods:

  • Bioinformatics analyses on T2DM database chip.
  • Establishment of a high glucose-induced T2DM cell model (RIN-m5F cells).
  • Assessment of PSMD3 gene function via overexpression, Western blotting, and flow cytometry.

Main Results:

  • PSMD3 methylation was upregulated in T2DM tissues and correlated with USP14.
  • PSMD3 overexpression decreased apoptosis and increased proliferation in high glucose-treated cells.
  • PSMD3 was linked to USP14 inactivation in high glucose-treated cells.

Conclusions:

  • PSMD3 methylation may influence T2DM development by affecting cell apoptosis and proliferation, potentially through USP14 activation.
  • This study enhances understanding of the molecular mechanisms underlying T2DM pathogenesis related to PSMD3 methylation.

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