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Previously, we have found that stromal cell\u2010derived factor 1\/<jats:styled-content style=\"fixed-case\">CXCR4<\/jats:styled-content> signaling is up\u2010regulated during wound healing in burn patients and <jats:styled-content style=\"fixed-case\">HTS<\/jats:styled-content> tissue after thermal injury. We hypothesize that blood\u2010borne mononuclear cells are recruited into wound sites after burn injury through the chemokine pathway of stromal cell\u2010derived factor 1 and its receptor <jats:styled-content style=\"fixed-case\">CXCR4<\/jats:styled-content>. Deep dermal injuries to the skin are often accompanied by prolonged inflammation, which leads to chemotaxis of mononuclear cells into the wounds by chemokine signaling where fibroblast activation occurs and ultimately <jats:styled-content style=\"fixed-case\">HTS<\/jats:styled-content> are formed. Blocking mononuclear cell recruitment and fibroblast activation, <jats:styled-content style=\"fixed-case\">CXCR4<\/jats:styled-content> antagonism is expected to reduce or minimize scar formation. In this study, the inhibitory effect of <jats:styled-content style=\"fixed-case\">CXCR4<\/jats:styled-content> antagonist <jats:styled-content style=\"fixed-case\">CTCE<\/jats:styled-content>\u20109908 on dermal fibrosis was determined in vivo using a human <jats:styled-content style=\"fixed-case\">HTS<\/jats:styled-content>\u2010like nude mouse model, in which split\u2010thickness human skin is transplanted into full\u2010thickness dorsal excisional wounds in athymic mice, where these wounds subsequently develop fibrotic scars that resemble human <jats:styled-content style=\"fixed-case\">HTS<\/jats:styled-content> as previously described. <jats:styled-content style=\"fixed-case\">CTCE<\/jats:styled-content>\u20109908 significantly attenuated scar formation and contraction, reduced the accumulation of macrophages and myofibroblasts, enhanced the remodeling of collagen fibers, and down\u2010regulated the gene and protein expression of fibrotic growth factors in the human skin tissues. These findings support the potential therapeutic value of <jats:styled-content style=\"fixed-case\">CXCR4<\/jats:styled-content> antagonist in dermal fibrosis and possibly other fibroproliferative disorders.<\/jats:p>","DOI":"10.1111\/wrr.12208","type":"journal-article","created":{"date-parts":[[2014,8,20]],"date-time":"2014-08-20T04:54:06Z","timestamp":1408510446000},"page":"622-630","source":"Crossref","is-referenced-by-count":28,"title":["The therapeutic potential of a <scp>C<\/scp>\u2010<scp>X<\/scp>\u2010<scp>C<\/scp> chemokine receptor type 4 (<scp>CXCR<\/scp>\u20104) antagonist on hypertrophic scarring in vivo"],"prefix":"10.1111","volume":"22","author":[{"given":"Jie","family":"Ding","sequence":"first","affiliation":[{"name":"Wound Healing Research Group Division of Plastic and Reconstructive Surgery University of Alberta  Edmonton Alberta 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