Linked Life Data

15252777

Source:http://linkedlifedata.com/resource/pubmed/id/15252777

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2004-7-14
pubmed:abstractText
This review discusses the concept that nitric oxide synthase (NOS) may orchestrate both the inflammatory response to the renal allograft and anti-inflammatory defense in the graft itself. NO is produced by endothelial, epithelial, as well as inflammatory cells. In the setting of transplantation, the endothelium is the first lining to be subjected to the early response to injury. In turn, activated endothelial cells facilitate leukocyte recruitment, immune-mediated injury, and angiogenesis. On activation by inflammatory stimuli, endothelial cells up-regulate multiple vasoactive substances, oxygen radicals, cytokines, chemokines, and growth factors. Therefore, endothelial integrity, especially the expression of protecting vasoactive agents, such as NO, may be a key factor in resistance or sensitivity to transplantation-mediated injury. Thus, evaluating the mechanisms by which NO is involved in either protecting or injuring the transplanted allogeneic kidney is important for our understanding of renal allograft rejection. This review focuses on the role of NO in the inflammatory endothelial-leukocyte interactions, which are implicated in acute and chronic rejection of the transplanted kidney.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0270-9295
pubmed:author
pubmed:issnType
Print
pubmed:volume
24
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
379-88
pubmed:dateRevised
2005-11-16
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
The role of nitric oxide in renal transplantation.
pubmed:affiliation
Department of Pathobiology, Division of Physiology, Leiden University Medical Center, The Netherlands. I.Vos@vet.uu.nl
pubmed:publicationType
Journal Article, Review