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

Moberg, Lisa ; Olsson, Annika ; Berne, Christian ; Felldin, Marie ; Foss, Aksel ; Källén, Ragnar LU ; Salmela, Kalja ; Tibell, Annika ; Tufveson, Gunnar and Nilsson, Bo , et al. (2003) In Transplantation 76(9). p.1285-1288
Abstract
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... (More)
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. (Less)
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publishing date
type
Contribution to journal
publication status
published
subject
in
Transplantation
volume
76
issue
9
pages
1285 - 1288
publisher
Lippincott Williams & Wilkins
external identifiers
  • wos:000186653100003
  • pmid:14627904
  • scopus:10744233687
ISSN
1534-6080
language
English
LU publication?
no
additional info
The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Hematology/Transplantation (013022014), Division of Hematology and Transfusion Medicine (013041100)
id
36dbb639-028b-4d60-9b1c-cc4f226f24e7 (old id 899754)
alternative location
http://www.transplantjournal.com/pt/re/transplantation/abstract.00007890-200311150-00003.htm
date added to LUP
2016-04-01 17:04:37
date last changed
2024-02-27 11:42:07
@article{36dbb639-028b-4d60-9b1c-cc4f226f24e7,
  abstract     = {{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.}},
  author       = {{Moberg, Lisa and Olsson, Annika and Berne, Christian and Felldin, Marie and Foss, Aksel and Källén, Ragnar and Salmela, Kalja and Tibell, Annika and Tufveson, Gunnar and Nilsson, Bo and Korsgren, Olle}},
  issn         = {{1534-6080}},
  language     = {{eng}},
  number       = {{9}},
  pages        = {{1285--1288}},
  publisher    = {{Lippincott Williams & Wilkins}},
  series       = {{Transplantation}},
  title        = {{Nicotinamide inhibits tissue factor expression in isolated human pancreatic islets: Implications for clinical islet transplantation}},
  url          = {{http://www.transplantjournal.com/pt/re/transplantation/abstract.00007890-200311150-00003.htm}},
  volume       = {{76}},
  year         = {{2003}},
}