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Nicotinamide inhibits tissue factor expression in isolated human pancreatic islets: Implications for clinical islet transplantation

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Author

  • Lisa Moberg
  • Annika Olsson
  • Christian Berne
  • Marie Felldin
  • Aksel Foss
  • Ragnar Källén
  • Kalja Salmela
  • Annika Tibell
  • Gunnar Tufveson
  • Bo Nilsson
  • Olle Korsgren
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Summary, in English

Background. Islet-produced tissue factor (TF) triggers an adverse clotting reaction, the instant blood-mediated inflammatory reaction (IBMIR), providing a likely explanation for the need of tissue from multiple donors in clinical islet transplantation. In this study, the authors investigated whether compounds previously shown to affect TF and macrophage chemoattractant protein (MCP)-1 expression in monocytes and endothelial cells have the same effect in human islet cells. Methods. Islets were cultured in the presence of L-arginine, cyclosporine A, enalapril, or nicotinamide for 48 hr, after which the TF content and MCP-1 expression were assessed. The effect of nicotinamide on IBMIR was evaluated by exposing the treated islets to fresh human ABO-compatible blood in an in vitro loop model. Results. Nicotinamide was the only compound that significantly reduced both TF and MCP-1. This reduction was dose-dependent. The level of MCP-1 was strongly correlated with TF expression (r(2)=0.98). In addition, the level of TF was also correlated with the ability of the islets to initiate IBMIR (r(2)=0.94). Conclusions. TF and MCP-1 expression in human islets can be decreased by adding nicotinamide to the culture medium. These observations indicate that the adverse effects of IBMIR in clinical islet transplantation could be reduced without endangering the recipient using antithrombotic drugs.

Publishing year

2003

Language

English

Pages

1285-1288

Publication/Series

Transplantation

Volume

76

Issue

9

Document type

Journal article

Publisher

Lippincott Williams & Wilkins

Topic

  • Surgery

Status

Published

ISBN/ISSN/Other

  • ISSN: 1534-6080