title: Interleukin (IL)-17A Promotes Angiogenesis in an Experimental Corneal Neovascularization Model.
abstract: To explore the roles of interleukin (IL)-17A in alkali-induced corneal neovascularization (CRNV).
  
  
  
  Induction of CRNV by alkali injury was performed and compared in recombinant mouse IL-17A protein or anti-mouse IL-17A neutralizing antibody (Ab)-treated mice. The expression of IL-17A, IL-17A receptor (IL-17RA), vascular endothelial growth factor (VEGF), IL-6, IL-8, and monocyte chemoattractant protein-1 (MCP-1) in burned corneas or other cells was examined by RT-PCR and western blot. The infiltration of macrophages, neutrophils, and c-Kit-positive progenitor cells into burned corneas was detected by flow cytometry (FCM). The Raw264.7 cell line and mouse corneal fibroblasts were stimulated by mouse recombinant IL-17A or anti-mouse IL-17A neutralizing Ab in vitro, and the expression of IL-6 and VEGF in culture supernatant was determined by enzyme-linked immunosorbent assay (ELISA).
  
  
  
  The alkali-induced CRNV peaked 2 weeks after the alkali burn. Compared with the vehicle-treated group, mouse recombinant IL-17A administration significantly increased the amount of CRNV, and it decreased in mice treated with neutralizing anti-mouse IL-17A Ab. RT-PCR and western blot confirmed that the IL-17A upregulated intracorneal VEGF, IL-6, IL-8, MCP-1, and phosphorylated focal adhesion kinase (pFAK) expression. FCM revealed that the infiltration of intracorneal progenitor cells, M1 macrophages, and neutrophils was also augmented in IL-17A-treated mice. The ELISA showed that IL-17A markedly induced VEGF and IL-6 expression in the Raw264.7 murine macrophage cell line and in the mouse corneal fibroblasts.
  
  
  
  IL-17A-treated mice exhibited enhanced alkali-induced CRNV through enhanced intracorneal progenitor cell and inflammatory cell infiltration, and increased VEGF and IL-6 expression by fibroblasts and macrophages.
authors.affiliation: a Department of Ophthalmology , The First Affiliated Hospital of Soochow University , Suzhou , P.R. China.|b Jiangsu Clinical Immunology Institute, The First Affiliated Hospital of Soochow University , Suzhou , P.R. China.
authors.forename: Gaoqin
authors.initials: G
authors.lastname: Liu
authors.affiliation: b Jiangsu Clinical Immunology Institute, The First Affiliated Hospital of Soochow University , Suzhou , P.R. China.
authors.forename: Hongya
authors.initials: H
authors.lastname: Wu
authors.affiliation: a Department of Ophthalmology , The First Affiliated Hospital of Soochow University , Suzhou , P.R. China.|b Jiangsu Clinical Immunology Institute, The First Affiliated Hospital of Soochow University , Suzhou , P.R. China.
authors.forename: Peirong
authors.initials: P
authors.lastname: Lu
authors.affiliation: b Jiangsu Clinical Immunology Institute, The First Affiliated Hospital of Soochow University , Suzhou , P.R. China.
authors.forename: Xueguang
authors.initials: X
authors.lastname: Zhang
mesh_terms: D000468:Alkalies / Q000633:toxicity; D000818:Animals; D015153:Blotting, Western; D002460:Cell Line; D003315:Cornea / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D016510:Corneal Neovascularization / Q000139:chemically induced / Q000188:drug therapy* / Q000235:genetics; D004195:Disease Models, Animal; D005347:Fibroblasts / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D005434:Flow Cytometry; D005786:Gene Expression Regulation; D007150:Immunohistochemistry; D020381:Interleukin-17 / Q000096:biosynthesis / Q000235:genetics* / Q000494:pharmacology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D012313:RNA / Q000235:genetics*; D011994:Recombinant Proteins / Q000494:pharmacology; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: D000468:Alkalies; C098680:Il17a protein, mouse; D020381:Interleukin-17; D011994:Recombinant Proteins; D012313:RNA
keywords: Chemokine; IL-17A; corneal; inflammation; neovascularization