Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2008-10-21
pubmed:abstractText
Transplant arteriopathy is the leading cause of long term morbidity and mortality following heart transplantation. Animal models have demonstrated that monocyte chemoattractant protein (MCP)-1 is induced early after transplant in cardiac and aortic allografts. We have previously reported that deficiency of MCP-1 or its receptor, CC chemokine receptor 2 (CCR2), is associated with a reduction in intimal proliferation in a mouse femoral artery injury model. Using knockout mice, we have now examined the role of MCP-1 and CCR2 in the development of the intimal proliferation of transplant arteriopathy.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1423-0135
pubmed:author
pubmed:copyrightInfo
Copyright 2008 S. Karger AG, Basel.
pubmed:issnType
Electronic
pubmed:volume
45
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
538-46
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Inhibition of MCP-1/CCR2 signaling does not inhibit intimal proliferation in a mouse aortic transplant model.
pubmed:affiliation
Aab Cardiovascular Research Institute, University of Rochester School of Medicine and Dentistry, Rochester, NY 14586, USA. jeffrey_alexis@urmc.rochester.edu
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't