ArticleThe American journal of pathology1996
Inducible and endothelial nitric oxide synthase expression during development of transplant arteriosclerosis in rat aortic grafts.
Article in The American journal of pathology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 70 citations in OpenAlex.
- Filamin B deficiency in mice results in skeletal malformations and impaired microvascular development.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- Increased plasma phenylacetic acid in patients with end-stage renal failure inhibits iNOS expression.The Journal of clinical investigation · 2003Article
- Prevention of the expression of inducible nitric oxide synthase by a novel positive inotropic agent, YS 49, in rat vascular smooth muscle and RAW 264.7 macrophages.British journal of pharmacology · 1999Article
- Tolerance induction ameliorates allograft vasculopathy in rat aortic transplants. Influence of Fas-mediated apoptosis.The Journal of clinical investigation · 1998Article
- Role of nitric oxide in experimental obliterative bronchiolitis (chronic rejection) in the rat.The Journal of clinical investigation · 1997Article
- Inducible nitric oxide synthase suppresses the development of allograft arteriosclerosis.The Journal of clinical investigation · 1997Article
- Inducible nitric oxide synthase expression in coronary arteries of transplanted human hearts with accelerated graft arteriosclerosis.The American journal of pathology · 1997Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the vascular system, distinct isoforms of nitric oxide synthase (NOS) generate nitric oxide (NO), which acts as a biological messenger. Its role in the development of transplant arteriosclerosis (TA) is still unclear. To investigate whether NO is involved in TA, we studied the expression of NOS isoforms, inducible NOS (iNOS) and endothelial NOS (eNOS), by immunohistochemistry and in situ hybridization during the first two post-transplantation months and their relation with cold ischemia (1 to 24 hours) and reperfusion injury using an aortic transplantation model in the rat. We found an increased iNOS expression in the intima and adventitia and a decreased expression in the media, whereas eNOS expression was not significantly altered during the development of TA. Co-localization studies suggested that iNOS-positive cells were vascular smooth muscle cells, monocyte-derived macrophages, and endothelial cells. Prolonged ischemic storage time resulted in an increase in eNOS expression in the neointima. In situ hybridization showed iNOS mRNA expression by vascular cells in the neointima and media. NO produced by iNOS and eNOS may be involved, at least in part, in the pathogenesis of TA in aortic grafts. Additional studies are needed to confirm the modulatory mechanism of NO during the development of TA.
Indexed as
Identifiers
8952533PMC1865349W1725843308What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.