title: Role of TGFBIp in Wound Healing and Mucin Expression in Corneal Epithelial Cells.
abstract: OBJECTIVE
  Transforming growth factor-β-induced protein (TGFBIp) is highly expressed in the cornea, and mutant TGFBIp induces corneal diseases. However, the function of TGFBIp in cornea epithelium is not fully investigated. Here, we tested the importance of TGFBIp in regulation of gene expression and corneal epithelial cell (CEC) activity.
  
  
  METHODS
  The effect of TGFBIp on CEC activity was analyzed by cell migration, adhesion, proliferation and wound healing assay. Analysis of gene expression was examined by western blot and quantitative reverse transcription PCR.
  
  
  RESULTS
  The results demonstrated that TGFBIp increased adhesion, migration, proliferation, and wound healing of CECs. Analysis of gene expression presented that TGFBIp-stimulated CECs exhibited increased expression of mucin family genes, such as MUC1, -4, -5AC, and -16. Furthermore, TGFBIp treatment increased the expression of MUC1, -4, -5AC, -7, and -16 in conjunctival epithelial cells. TGFBIp also increased the activity of intracellular signaling molecules ERK and AKT in CECs. Using pharmacologic inhibitors of ERK and AKT, we showed that the expression of mucin genes by TGFBIp is mediated by the activation of ERK and AKT signaling.
  
  
  CONCLUSIONS
  Our findings demonstrate that the locally generated TGFBIp in the cornea may contribute to wound healing of CECs by enhancing the migration, adhesion, and proliferation of CECs. In addition, our results suggest that TGFBIp has a protective effect on ocular surfaces by inducing the expression of mucin genes in corneal and conjunctival epithelial cells. These data suggest that TGFBIp is a useful therapeutic target for patients with corneal wounds.
authors.affiliation: Department of Ophthalmology, Corneal Dystrophy Research Institute, Yonsei University College of Medicine, Seoul, Korea.
authors.forename: Yong Sun
authors.initials: YS
authors.lastname: Maeng
authors.affiliation: Department of Ophthalmology, Corneal Dystrophy Research Institute, Yonsei University College of Medicine, Seoul, Korea.
authors.forename: Ga Hyun
authors.initials: GH
authors.lastname: Lee
authors.affiliation: Department of Ophthalmology, Corneal Dystrophy Research Institute, Yonsei University College of Medicine, Seoul, Korea.
authors.forename: Boram
authors.initials: B
authors.lastname: Lee
authors.affiliation: Department of Ophthalmology, Corneal Dystrophy Research Institute, Yonsei University College of Medicine, Seoul, Korea.
authors.forename: Seung Il
authors.initials: SI
authors.lastname: Choi
authors.affiliation: Department of Ophthalmology, Corneal Dystrophy Research Institute, Yonsei University College of Medicine, Seoul, Korea.
authors.forename: Tae Im
authors.initials: TI
authors.lastname: Kim
authors.affiliation: Department of Ophthalmology, Corneal Dystrophy Research Institute, Yonsei University College of Medicine, Seoul, Korea.|Institute of Vision Research, Severance Biomedical Science Institute, Yonsei University College of Medicine, Seoul, Korea. eungkkim@yuhs.ac.
authors.forename: Eung Kweon
authors.initials: EK
authors.lastname: Kim
mesh_terms: D015153:Blotting, Western; D002448:Cell Adhesion; D002465:Cell Movement / Q000187:drug effects; D049109:Cell Proliferation; D002478:Cells, Cultured; D003228:Conjunctiva / Q000166:cytology; D003315:Cornea / Q000166:cytology*; D004847:Epithelial Cells / Q000378:metabolism*; D016326:Extracellular Matrix Proteins / Q000502:physiology*; D015870:Gene Expression; D006801:Humans; D009077:Mucins / Q000235:genetics / Q000378:metabolism*; D015398:Signal Transduction; D016212:Transforming Growth Factor beta / Q000502:physiology*; D014945:Wound Healing / Q000502:physiology*; D000099222:betaIG-H3 Protein
chemical_list: D016326:Extracellular Matrix Proteins; D009077:Mucins; D016212:Transforming Growth Factor beta; D000099222:betaIG-H3 Protein
keywords: TGFBIp; cornea; epithelial cells; mucin