Linked Life Data

20561305

Source:http://linkedlifedata.com/resource/pubmed/id/20561305

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2010-11-9
pubmed:abstractText
Chronic rejection (CR) remains an unsolved hurdle for long-term heart transplant survival. The effect of cold ischemia (CI) on progression of CR and the mechanisms resulting in functional deficit were investigated by studying gene expression, mitochondrial function, and enzymatic activity. Allogeneic (Lew?F344) and syngeneic (Lew?Lew) heart transplantations were performed with or without 10 h of CI. After evaluation of myocardial contraction, hearts were excised at 2, 10, 40, and 60 days for investigation of vasculopathy, gene expression, enzymatic activities, and mitochondrial respiration. Gene expression studies identified a gene cluster coding for subunits of the mitochondrial electron transport chain regulated in response to CI and CR. Myocardial performance, mitochondrial function, and mitochondrial marker enzyme activities declined in all allografts with time after transplantation. These declines were more rapid and severe in CI allografts (CR-CI) and correlated well with progression of vasculopathy and fibrosis. Mitochondria related gene expression and mitochondrial function are substantially compromised with the progression of CR and show that CI impacts on progression, gene profile, and mitochondrial function of CR. Monitoring mitochondrial function and enzyme activity might allow for earlier detection of CR and cardiac allograft dysfunction.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1432-2277
pubmed:author
pubmed:copyrightInfo
© 2010 The Authors. Journal compilation © 2010 European Society for Organ Transplantation.
pubmed:issnType
Electronic
pubmed:volume
23
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1282-92
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Cold ischemia contributes to the development of chronic rejection and mitochondrial injury after cardiac transplantation.
pubmed:affiliation
Daniel Swarovski Research Laboratory, Department of Visceral, Transplant and Thoracic Surgery, Center of Operative Medicine, Innsbruck Medical University, Anichstrasse 35, Innsbruck, Austria. stefan.schneeberger@i-med.ac.at
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't