title: Deletion of the FHL2 gene attenuating neovascularization after corneal injury.
abstract: OBJECTIVE
  The four-and-one-half LIM domain-containing protein2 (FHL2) is a member of the four-and-a-half LIM domain-only (FHL) gene family. Although FHL2 is expressed in the cornea, its role in angiogenesis is unclear. The aim of this study was to investigate the role of the FHL2 gene in corneal angiogenesis after chemical injury.
  
  
  METHODS
  FHL2-LacZ knock-in mice were used to trace FHL2 gene expression before and after corneal injury. Corneal angiogenesis between FHL2-null mice and wild-type mice that underwent chemical and mechanical denudation of corneal and limbal epithelium were compared. New growth vessel density was assessed by CD31 staining and was analyzed using image analysis software. Levels of vascular endothelial growth factor (VEGF) and cyclooxygenase (COX)-2 proteins were determined by Western blot assay.
  
  
  RESULTS
  beta-Galactosidase staining of corneal tissue in FHL2-LacZ knock-in mice revealed that FHL2 gene expression is upregulated in the corneal epithelium after corneal injury. Ten days after injury, corneal neovascularization was observed in control and FHL2-null mice. New corneal vessel density was found to be lower in the FHL2-null mice injury group than in the wild-type mice injury group. Western blot analysis showed that VEGF and COX-2 protein levels were higher after chemical injury in FHL2-null mice and wild-type mice. However, the upregulated VEGF protein was significantly lower in the FHL2-null mice than in the wild-type mice.
  
  
  CONCLUSIONS
  The decreased chemical-induced corneal angiogenesis found in the FHL2-null mice in this study indicated that FHL2 protein plays a role in inhibiting inflammatory angiogenesis.
authors: First Cardiovascular Division, Department of Internal Medicine, Chang-Gung Memorial Hospital, Chang-Gung University College of Medicine, Taipei, Taiwan. pchu@adm.cgmh.org.tw
authors: Pao-Hsien
authors: PH
authors: Chu
authors: Lung-Kun
authors: LK
authors: Yeh
authors: Hsin-Chiung
authors: HC
authors: Lin
authors: Shih-Ming
authors: SM
authors: Jung
authors: David Hui-Kang
authors: DH
authors: Ma
authors: I-Jong
authors: IJ
authors: Wang
authors: Hsueh-Hua
authors: HH
authors: Wu
authors: Tzu-Fang
authors: TF
authors: Shiu
authors: Ju
authors: J
authors: Chen
mesh_terms: D000818:Animals; D015153:Blotting, Western; D002057:Burns, Chemical / Q000209:etiology; D065306:Corneal Injuries; D016510:Corneal Neovascularization / Q000235:genetics / Q000473:pathology / Q000517:prevention & control*; D051546:Cyclooxygenase 2 / Q000378:metabolism; D004195:Disease Models, Animal; D005126:Eye Burns / Q000139:chemically induced* / Q000378:metabolism; D017353:Gene Deletion; D005786:Gene Expression Regulation / Q000502:physiology; D018398:Homeodomain Proteins / Q000235:genetics*; D060850:LIM-Homeodomain Proteins; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009124:Muscle Proteins / Q000235:genetics*; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000378:metabolism; D012972:Sodium Hydroxide; D014157:Transcription Factors / Q000235:genetics*; D015854:Up-Regulation; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism
chemical_list: C491382:Fhl2 protein, mouse; D018398:Homeodomain Proteins; D060850:LIM-Homeodomain Proteins; D009124:Muscle Proteins; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D014157:Transcription Factors; D042461:Vascular Endothelial Growth Factor A; C467480:vascular endothelial growth factor A, mouse; D012972:Sodium Hydroxide; C077623:Ptgs2 protein, mouse; D051546:Cyclooxygenase 2