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Heparanase and Type 1 Diabetes.

Charmaine J Simeonovic1, Sarah K Popp2, Debra J Brown2

  • 1Department of Immunology and Infectious Disease, The John Curtin School of Medical Research, The Australian National University, Canberra, ACT, Australia. Charmaine.Simeonovic@anu.edu.au.

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Heparanase enzyme activity degrades heparan sulfate (HS), driving Type 1 diabetes (T1D) progression by enabling immune cell invasion and beta cell destruction. Inhibiting heparanase and replacing HS shows promise for T1D treatment.

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Area of Science:

  • Immunology and Endocrinology
  • Molecular Biology and Glycobiology

Background:

  • Type 1 diabetes (T1D) involves autoimmune destruction of pancreatic beta cells.
  • Heparan sulfate (HS) degradation by heparanase is implicated in T1D pathogenesis.
  • Highly sulfated HS is crucial for beta cell viability and function.

Purpose of the Study:

  • To elucidate the role of heparanase in T1D development and progression.
  • To investigate heparanase inhibitors and HS mimetics as potential T1D therapeutics.

Main Methods:

  • Analysis of heparanase expression in T1D models (NOD mice) and human T1D patients.
  • Assessment of HS degradation in pancreatic islets during T1D progression.
  • In vivo efficacy study of heparanase inhibitor PI-88 in NOD mice.

Main Results:

  • Heparanase facilitates leukocyte infiltration into islets and beta cell destruction.
  • T1D progression correlates with increased heparanase expression in myeloid leukocytes.
  • PI-88 treatment reduced T1D incidence by 50%, inhibited insulitis, and preserved beta cell HS.

Conclusions:

  • Heparanase is a key mediator of T1D, distinct from T cell-mediated cytotoxicity.
  • Dual-action heparanase inhibitors/HS replacers represent a novel therapeutic strategy for T1D.
  • This approach may also mitigate secondary vascular complications associated with diabetes.