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Early differences in islets from prediabetic NOD mice: combined microarray and proteomic analysis.

Inne Crèvecoeur1, Valborg Gudmundsdottir2, Saurabh Vig1

  • 1Laboratory for Clinical and Experimental Endocrinology, KU Leuven, Herestraat 49 bus 902, 3000, Leuven, Belgium.

Diabetologia
|January 13, 2017
PubMed
Summary
This summary is machine-generated.

Type 1 diabetes may start within pancreatic islets before immune cell attack. Intrinsic beta cell changes, including protein misfolding and citrullination, may trigger the autoimmune process, contributing to disease initiation.

Keywords:
2D-DIGEBeta cellsIntrinsic differencesMicroarrayNOD micePathway analysisPost-translational modificationsType 1 diabetes

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Area of Science:

  • Endocrinology
  • Immunology
  • Molecular Biology

Background:

  • Type 1 diabetes (T1D) is an endocrine disease with a prolonged preclinical phase characterized by insulitis.
  • While immune system involvement is studied, the role of beta cells in T1D initiation is less understood.

Purpose of the Study:

  • To investigate intrinsic differences in pancreatic islets from diabetes-prone NOD mice before insulitis onset.
  • To explore the potential contribution of beta cells to the autoimmune process in T1D.

Main Methods:

  • Transcriptome analysis using microarray.
  • Proteome analysis using 2D-DIGE.
  • Pathway and gene/protein expression analysis for T1D relevance.

Main Results:

  • Alterations in metabolism and cell communication pathways were observed in the preinsulitic period.
  • Post-translational modifications (PTMs), particularly citrullination by PAD2, were implicated.
  • Protein misfolding due to low expression of protein disulphide isomerases (PDIA3, 4, 6) was identified as a factor inducing beta cell stress and auto-antigen generation.

Conclusions:

  • Pancreatic islets may contribute to the initiation of the autoimmune process in T1D, independent of immune cell differences.
  • Intrinsic beta cell stress and auto-antigen generation are potential early mechanisms in T1D pathogenesis.