Role of inducible nitric oxide synthase in transplant arteriosclerosis.

Abstract

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.

• Authors: P C Lee, L L Shears 2nd, T R Billiar
• Journal: Clinical and experimental pharmacology & physiology (Clin Exp Pharmacol Physiol) Vol. 26 Issue 12 Pg. 1013-5 (Dec 1999) ISSN: 0305-1870 [Print] Australia
• PMID: 10626073 (Publication Type: Journal Article, Review)

Chemical References

• NOS2 protein, human
• Nitric Oxide Synthase
• Nitric Oxide Synthase Type II

Topics

• Animals
• Arteriosclerosis (enzymology, etiology)
• Humans
• Nitric Oxide Synthase (physiology)
• Nitric Oxide Synthase Type II
• Transplantation, Homologous (adverse effects)