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J. Biol. Chem., Vol. 275, Issue 47, 36509-36513, November 24, 2000
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From the Departments of Interleukin-1
Protection of Human Islets from the Effects of Interleukin-1
by Adenoviral Gene Transfer of an I
B Repressor*
§,
Molecular Genetics and
Biochemistry and of ¶ Pediatrics, University of Pittsburgh School
of Medicine, Pittsburgh, Pennsylvania 15261
(IL-1) is a pro-inflammatory
cytokine that inhibits cell function and promotes Fas-triggered
apoptosis. IL-1 is thought to act early in the initiation of the
autoimmune destruction of pancreatic cells in type I diabetes.
IL-1 promotes cell impairment, in part, by activating NF-
B
transcription factor-dependent signaling pathways. We have
examined whether cells could be protected from the effects of
IL-1 by overexpressing an inhibitor of NF-B activity, IB, by
adenoviral gene transfer to intact human islets in culture. Infection
of islets with an adenoviral vector encoding a non-phosphorylatable,
non-degradable variant of IB
resulted in normal insulin responses
to glucose in the presence of IL-1. Furthermore, nitric oxide
production was prevented and, more importantly, Fas-triggered apoptosis
was inhibited following IB gene transfer. These results suggest that blocking the NF-B pathway might prevent cytokine-induced cell impairment as a means of facilitating islet transplantation.
*
This work was supported in part by a program project grant
from the Juvenile Diabetes Foundation International (to M. T. and P. D. R.).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed: Dept. of Molecular
Genetics and Biochemistry, W1246 BST, University of Pittsburgh School
of Medicine, Pittsburgh, PA 15261. Tel.: 412-648-9268; Fax:
412-383-8837; E-mail: probb@pitt.edu.
Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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