Abstract:
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]
journal_name
Diabetologiajournal_title
Diabetologiaauthors
Chen MC,Schuit F,Eizirik DLdoi
10.1007/s001250051292subject
Has Abstractpub_date
1999-10-01 00:00:00pages
1199-203issue
10eissn
0012-186Xissn
1432-0428pii
90421199.125journal_volume
42pub_type
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