ROLE OF INDUCIBLE NITRIC OXIDE SYNTHASE IN TRANSPLANT ARTERIOSCLEROSIS

SUMMARY 1. Transplant arteriosclerosis is a major obstacle to long‐term allograft survival. Nitric oxide (NO) has been implicated as a mediator in the development of this disease. 2. We and others have shown that inducible nitric oxide synthase (iNOS) is up‐regulated in allografts with transplant ar...

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Bibliographic Details
Published in:Clinical and experimental pharmacology & physiology 1999-12, Vol.26 (12), p.1013-1015
Main Authors: Lee, Paul C, Shears II, Larry L Shears, Billiar, Timothy R
Format: Article
Language:English
Subjects:
allografts
Animals
Arteriosclerosis - enzymology
Arteriosclerosis - etiology
gene therapy
gene transfer
Humans
inducible nitric oxide synthase
intimal hyperplasia
nitric oxide
Nitric Oxide Synthase - physiology
Nitric Oxide Synthase Type II
transplant arteriosclerosis
transplant vasculopathy
Transplantation, Homologous - adverse effects
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Summary:SUMMARY 1. Transplant arteriosclerosis is a major obstacle to long‐term allograft survival. Nitric oxide (NO) has been implicated as a mediator in the development of this disease. 2. We and others have shown that inducible nitric oxide synthase (iNOS) is up‐regulated in allografts with transplant arteriosclerosis. Despite the acute cytotoxic effects produced by high levels of NO, a chronic increase in NO availability is protective against neointimal hyperplasia, mainly by suppressing the inflammatory cell recruitment and neointimal smooth muscle cell accumulation. 3. Currently, we have the technology to directly transfer the iNOS gene to allografts. We have demonstrated that this exciting strategy is feasible and therapeutic and may improve the long‐term survival and function of allografts. Future challenges include optimizing the methods and the vectors of gene delivery.
ISSN:0305-1870
1440-1681
DOI:10.1046/j.1440-1681.1999.03183.x