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http://purl.uniprot.org/citations/18776949http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/18776949http://www.w3.org/2000/01/rdf-schema#comment"

Purpose

To evaluate the roles of CCL3 and its specific chemokine receptors, CCR1 and CCR5, in alkali-induced corneal neovascularization (CNV).

Methods

Chemical denudation of corneal and limbal epithelium was performed on wild-type (WT) BALB/c mice and CCL3-, CCR1-, and CCR5-deficienct (knockout [KO]) counterparts. Two weeks after injury CNV was quantified by immunostaining with anti-CD31. Angiogenic factor expression and leukocyte accumulation in the early phase after injury were quantified by reverse transcription polymerase chain reaction (RT-PCR) and immunohistochemical analysis, respectively.

Results

Alkali injury augmented the intraocular mRNA expression of CCL3 and its receptors, CCR1 and CCR5, together with a transient infiltration of F4/80 positive macrophages and Gr-1 positive neutrophils. Compared with WT mice, CCL3-KO and CCR5-KO mice but not CCR1-KO mice exhibited reduced CNV two weeks after injury both macroscopically and microscopically as evidenced by CD31 positive areas. Concomitantly, the infiltration of F4/80 positive macrophages but not Gr-1 positive neutrophils was significantly attenuated in CCL3-KO mice compared with WT mice. Intracorneal infiltration of CCR5 expressing cells was significantly impaired in CCL3-KO mice compared with WT mice. Alkali injury induced a massive increase in the intraocular mRNA expression of a potent angiogenic factor, vascular endothelial growth factor (VEGF), in WT mice whereas these increments were severely retarded in CCL3-KO mice. Moreover, CCL3 enhanced VEGF expression by murine peritoneal macrophages at both the mRNA and the protein level. Furthermore, topical CCL3 application restored CNV, which was macroscopically and microscopically reduced in CCL3-KO mice after two weeks to levels similar to those found in WT mice.

Conclusions

In alkali-induced CNV, CCL3 induced macrophages to infiltrate and produce VEGF by binding to CCR5 but not to CCR1 and eventually promoted angiogenesis."xsd:string
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http://purl.uniprot.org/citations/18776949http://purl.uniprot.org/core/author"Wu Y."xsd:string
http://purl.uniprot.org/citations/18776949http://purl.uniprot.org/core/author"Zhang X."xsd:string
http://purl.uniprot.org/citations/18776949http://purl.uniprot.org/core/author"Lu P."xsd:string
http://purl.uniprot.org/citations/18776949http://purl.uniprot.org/core/author"Mukaida N."xsd:string
http://purl.uniprot.org/citations/18776949http://purl.uniprot.org/core/date"2008"xsd:gYear
http://purl.uniprot.org/citations/18776949http://purl.uniprot.org/core/name"Mol Vis"xsd:string
http://purl.uniprot.org/citations/18776949http://purl.uniprot.org/core/pages"1614-1622"xsd:string
http://purl.uniprot.org/citations/18776949http://purl.uniprot.org/core/title"Essential contribution of CCL3 to alkali-induced corneal neovascularization by regulating vascular endothelial growth factor production by macrophages."xsd:string
http://purl.uniprot.org/citations/18776949http://purl.uniprot.org/core/volume"14"xsd:string
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