Identification of IL-1beta-induced messenger RNAs in rat pancreatic beta cells by differential display of messenger RNA

Diabetologia. 1999 Oct;42(10):1199-203. doi: 10.1007/s001250051292.


Aims/hypothesis: Interleukin-1beta is a putative mediator of pancreatic beta-cell dysfunction and damage in Type I (insulin-dependent) diabetes mellitus. To better understand the molecular mechanisms involved in IL-1beta effects, we carried out a differential display of mRNA by RT-PCR to identify novel cytokine-regulated genes.

Methods: Fluorescence activated cell sorting-purified rat pancreatic beta-cells were exposed for 6 or 24 h to IL-1beta. Differentially expressed cDNA bands were cloned and then identified by comparing their sequences with data from the GenBank. Differential gene expression was confirmed by RT-PCR using specific primers.

Results: Interleukin-1beta increased the expression of adenine nucleotide translocator-1, phospholipase D-1 and cytokine-induced neutrophil chemoattractant-1 and decreased expression of the protein tyrosine phosphatase-like protein IA-2. Interleukin-1beta-induced differential expression of these genes in beta cells was confirmed by RT-PCR. In additional studies, IL-1beta was shown to induce chemokines other than cytokine-induced neutrophil chemoattractant-1, including cytokine-induced neutrophil chemoattractant-3 and monocyte chemotactic protein-1.

Conclusion/interpretation: Our observations indicate that IL-1beta modifies the expression of several genes in pancreatic beta cells. These genes may affect both function, viability and beta-cell recognition by the immune system. Functional characterization of the mRNAs which have been identified could facilitate a better understanding of the mechanisms leading to beta-cell destruction in Type I diabetes. [Diabetologia (1999) 42: 1199-1203]

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Autoantigens
  • Chemokine CCL2 / genetics
  • Chemokine CCL2 / metabolism
  • Chemokine CXCL1
  • Chemokines, CXC*
  • Chemotactic Factors / genetics
  • Chemotactic Factors / metabolism
  • Gene Expression / drug effects
  • Growth Substances / genetics
  • Growth Substances / metabolism
  • Intercellular Signaling Peptides and Proteins*
  • Interleukin-1 / pharmacology*
  • Islets of Langerhans / drug effects*
  • Islets of Langerhans / metabolism*
  • Male
  • Membrane Glycoproteins / genetics
  • Membrane Glycoproteins / metabolism
  • Membrane Proteins / genetics
  • Membrane Proteins / metabolism
  • Mitochondrial ADP, ATP Translocases / genetics
  • Mitochondrial ADP, ATP Translocases / metabolism
  • Nitric Oxide Synthase / genetics
  • Nitric Oxide Synthase / metabolism
  • Nitric Oxide Synthase Type II
  • Phospholipase D / genetics
  • Phospholipase D / metabolism
  • Protein Tyrosine Phosphatases / genetics
  • Protein Tyrosine Phosphatases / metabolism
  • RNA, Messenger / biosynthesis*
  • Rats
  • Receptor-Like Protein Tyrosine Phosphatases, Class 8
  • Reverse Transcriptase Polymerase Chain Reaction


  • Autoantigens
  • CXCL1 protein, human
  • Chemokine CCL2
  • Chemokine CXCL1
  • Chemokines, CXC
  • Chemotactic Factors
  • Cxcl1 protein, rat
  • Growth Substances
  • Intercellular Signaling Peptides and Proteins
  • Interleukin-1
  • Membrane Glycoproteins
  • Membrane Proteins
  • RNA, Messenger
  • Mitochondrial ADP, ATP Translocases
  • Nitric Oxide Synthase
  • Nitric Oxide Synthase Type II
  • Nos2 protein, rat
  • PTPRN protein, human
  • PTPRN2 protein, human
  • Protein Tyrosine Phosphatases
  • Ptprn protein, rat
  • Receptor-Like Protein Tyrosine Phosphatases, Class 8
  • Phospholipase D
  • phospholipase D1