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The chemokine receptor CCR1 is strongly up‐regulated after skin injury but dispensable for wound healing
Author(s) -
Kaesler Susanne,
Bug Philippe,
Gao JiLiang,
Murphy Philip M.,
Goppelt Andreas,
Werner Sabine
Publication year - 2004
Publication title -
wound repair and regeneration
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.847
H-Index - 109
eISSN - 1524-475X
pISSN - 1067-1927
DOI - 10.1111/j.1067-1927.2004.012112.x
Subject(s) - ctgf , hepatic stellate cell , fibrosis , sirius red , connective tissue , wound healing , cancer research , ccl4 , chemistry , transforming growth factor beta , growth factor , pathology , biology , microbiology and biotechnology , transforming growth factor , carbon tetrachloride , endocrinology , immunology , receptor , medicine , biochemistry , organic chemistry
To identify key regulators of cutaneous wound repair, we analyzed a subtractive cDNA library of normal and wounded mouse skin. One of the identified genes encodes the chemokine receptor CCR1, which binds several chemokines present at the wound site. Expression of CCR1 was barely detectable in nonwounded skin, but strong up‐regulation was observed after injury to wild‐type mice. Most important, the healing abnormalities observed in glucocorticoid‐treated mice and activin‐overexpressing transgenic mice correlated with an altered expression of CCR1. CCR1‐positive cells were identified as macrophages and neutrophils within the wounded area. To determine the importance of CCR1 for wound repair, we analyzed this process in CCR1 knockout mice. Surprisingly, no alterations in either wound closure, wound appearance, wound bursting strength, granulation tissue formation, or re‐epithelialization were observed. In addition, the inflammatory response was unaltered in CCR1‐deficient mice and the expression of several chemokines, chemokine receptors, and other important regulators of wound repair were normal in these animals. These results show that CCR1 is dispensable for wound healing, most likely due to redundancy in chemokine/chemokine receptor signaling.