Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2010-3-29
pubmed:abstractText
CXC chemokine receptor 3 (CXCR3) signaling promotes keratinocyte migration while terminating fibroblast and endothelial cell immigration into wounds; this signaling also directs epidermal and matrix maturation. Herein, we investigated the long-term effects of failure to activate the "stop-healing" CXCR3 axis. Full-thickness excisional wounds were created on CXCR3 knockout((-/-)) or wild-type mice and examined at up to 180 days after wounding. Grossly, the CXCR3(-/-) mice presented a thick keratinized scar compared with the wild-type mice in which the scar was scarcely noticeable; histological examination revealed thickening of both the epidermis and dermis. The dermis was disorganized with thick and long collagen fibrils and contained excessive collagen content in comparison with the wild-type mice. Interestingly, the CXCR3(-/-) wounds presented lower tensile/burst strength, which correlates with decreased alignment of collagen fibers, similar to published findings of human scars. Persistent Extracellular matrix turnover and immaturity was shown by the elevated expression of proteins of the immature matrix as well as expression of matrix metallopeptidase-9 MMP-9. Interestingly, the scars in the CXCR3(-/-) mice presented evidence of de novo development of a sterile inflammatory response only months after wounding; earlier periods showed resolution of the initial inflammatory stage. These in vivo studies establish that the absence of CXCR3(-/-) signaling network results in hypertrophic and hypercellular scarring characterized by on-going wound regeneration, cellular proliferation, and scars in which immature matrix components are undergoing increased turnover resulting in a chronic inflammatory process.
pubmed:commentsCorrections
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pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1525-2191
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
176
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1743-55
pubmed:dateRevised
2011-7-27
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Lack of CXC chemokine receptor 3 signaling leads to hypertrophic and hypercellular scarring.
pubmed:affiliation
University of Pittsburgh, Department of Pathology, Pittsburgh, PA 15261, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural