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Methods to Assess Beta Cell Death Mediated by Cytotoxic T Lymphocytes
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Published on: June 16, 2011

Immune-mediated beta-cell destruction in vitro and in vivo-A pivotal role for galectin-3

Allan E Karlsen1, Zenia M Størling, Thomas Sparre

  • 1Steno Diabetes Center, Gentofte, Denmark. aek@novonordisk.com

Biochemical and Biophysical Research Communications
|April 8, 2006
PubMed

Pro-apoptotic cytokines are toxic to the pancreatic beta-cells and have been associated with the pathogenesis of Type 1 diabetes (T1D). Proteome analysis of IL-1beta exposed isolated rat islets identified galectin-3 (gal-3) as the most up-regulated protein. Here analysis of human and rat islets and insulinoma cells confirmed IL-1beta regulated gal-3 expression of several gal-3 isoforms and a complex in vivo expression profile during diabetes development in rats. Over-expression of gal-3 protected beta-cells against IL-1beta toxicity, with a complete blockage of JNK phosphorylation, essential for IL-1-mediated apoptosis. Mutation scanning of regulatory and coding regions of the gal-3 gene (LGALS3) identified six polymorphisms. A haplotype comprising three cSNPs showed significantly increased transmission to unaffected offspring in 257 T1D families and replicated in an independent set of 170 T1D families. In summary, combined proteome-transcriptome-genome and functional analyses identify gal-3 as a candidate gene/protein in T1D susceptibility that may prove valuable in future intervention/prevention strategies.

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