title: Critical role of SDF-1α-induced progenitor cell recruitment and macrophage VEGF production in the experimental corneal neovascularization.
abstract: OBJECTIVE
  To address the roles of the stromal derived factor-1 (SDF-1) α in the course of experimental corneal neovascularization (CNV).
  
  
  METHODS
  CNV was induced by alkali injury and compared in SDF-1α- or vehicle-treated mice two weeks after injury. Angiogenic factor expression in the early phase after injury was quantified by reverse transcription polymerase chain reaction (RT-PCR). Progenitor cell, macrophage, and monocyte intracorneal accumulation in the early phase after injury was evaluated by flow cytometric analysis.
  
  
  RESULTS
  The mRNA expression of SDF-1α was augmented, together with infiltration of c-kit-positive progenitor cells in the corneas after the alkali injury. Compared with vehicle-treated mice, SDF-1α-treated mice exhibited enhanced CNV two weeks after injury, as evidenced by enlarged cluster of differentiation 31 (CD31)-positive areas. Concomitantly, the intracorneal infiltration of c-kit-positive progenitor cells but not F4/80+ macrophages or Ly-6G+ monocytes was significantly enhanced in SDF-1α-treated mice compared to vehicle-treated mice. SDF-1α enhanced vascular endothelial growth factor (VEGF) expression by murine peritoneal macrophages. Enhancement in intraocular VEGF expression was greater in SDF-1α-treated mice than in control mice after injury. Moreover, local administration of C-X-C chemokine receptor type 4 (CXCR4) antagonist after alkali injury reduced alkali-induced CNV.
  
  
  CONCLUSIONS
  SDF-1α-treated mice exhibited enhanced alkali-induced CNV through enhanced intracorneal progenitor cell infiltration and increased VEGF expression by macrophages.
authors.affiliation: Department of Ophthalmology, the First Affiliated Hospital of Soochow University, Suzhou, P.R. China.
authors.forename: Gaoqin
authors.initials: G
authors.lastname: Liu
authors.forename: Peirong
authors.initials: P
authors.lastname: Lu
authors.forename: Longbiao
authors.initials: L
authors.lastname: Li
authors.forename: Hui
authors.initials: H
authors.lastname: Jin
authors.forename: Xuefei
authors.initials: X
authors.lastname: He
authors.forename: Naofumi
authors.initials: N
authors.lastname: Mukaida
authors.forename: Xueguang
authors.initials: X
authors.lastname: Zhang
mesh_terms: D000287:Administration, Topical; D000468:Alkalies / Q000009:adverse effects; D043925:Angiogenesis Inducing Agents / Q000276:immunology / Q000378:metabolism; D000818:Animals; D002465:Cell Movement / Q000187:drug effects*; D054377:Chemokine CXCL12 / Q000009:adverse effects / Q000494:pharmacology; D003315:Cornea / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D016510:Corneal Neovascularization / Q000139:chemically induced / Q000276:immunology / Q000378:metabolism* / Q000473:pathology*; D004195:Disease Models, Animal; D005434:Flow Cytometry; D006801:Humans; D008264:Macrophages / Q000276:immunology / Q000378:metabolism; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D009000:Monocytes / Q000276:immunology / Q000378:metabolism; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000032:analysis; D012333:RNA, Messenger / Q000032:analysis / Q000096:biosynthesis; D019718:Receptors, CXCR4 / Q000037:antagonists & inhibitors / Q000276:immunology / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015398:Signal Transduction / Q000187:drug effects*; D013234:Stem Cells / Q000276:immunology / Q000378:metabolism; D042461:Vascular Endothelial Growth Factor A / Q000096:biosynthesis* / Q000276:immunology
chemical_list: D000468:Alkalies; D043925:Angiogenesis Inducing Agents; D054377:Chemokine CXCL12; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D012333:RNA, Messenger; D019718:Receptors, CXCR4; D042461:Vascular Endothelial Growth Factor A