Role of TGFBIp in Wound Healing and Mucin Expression in Corneal Epithelial Cells.
10.3349/ymj.2017.58.2.423
- Author:
Yong Sun MAENG
1
;
Ga Hyun LEE
;
Boram LEE
;
Seung Il CHOI
;
Tae Im KIM
;
Eung Kweon KIM
Author Information
1. Department of Ophthalmology, Corneal Dystrophy Research Institute, Yonsei University College of Medicine, Seoul, Korea. eungkkim@yuhs.ac
- Publication Type:Original Article
- Keywords:
TGFBIp;
mucin;
cornea;
epithelial cells
- MeSH:
Blotting, Western;
Cell Movement;
Cornea;
Corneal Diseases;
Epithelial Cells*;
Epithelium;
Gene Expression;
Gene Expression Regulation;
Humans;
Mucins*;
Polymerase Chain Reaction;
Reverse Transcription;
Wound Healing*;
Wounds and Injuries*
- From:Yonsei Medical Journal
2017;58(2):423-431
- CountryRepublic of Korea
- Language:English
-
Abstract:
PURPOSE: 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. MATERIALS AND 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. CONCLUSION: 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.
