RGD Reference Report - TGF-beta receptor types I and II are differentially expressed during corneal epithelial wound repair. - Rat Genome Database

RGD Reference Report - TGF-beta receptor types I and II are differentially expressed during corneal epithelial wound repair. - Rat Genome Database

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TGF-beta receptor types I and II are differentially expressed during corneal epithelial wound repair.
Authors:	Zieske, JD Hutcheon, AE Guo, X Chung, EH Joyce, NC
Citation:	Zieske JD, etal., Invest Ophthalmol Vis Sci. 2001 Jun;42(7):1465-71.
RGD ID:	1601603
Pubmed:	PMID:11381048 (View Abstract at PubMed)
PURPOSE: It has been demonstrated that cells migrating to cover an epithelial debridement wound exit the cell cycle and that the cell-cycle inhibitor p15(INK4b) is upregulated in these cells. TGF-beta signaling has been implicated in both of these processes, and this study was conducted to determine whether the expression and localization of TGF-beta receptor (TbetaR)-I and -II are altered during corneal epithelial wound repair. METHODS: Three-millimeter superficial keratectomy wounds and 3-mm debridement wounds were made in central rat cornea and allowed to heal in vivo for 1 to 48 hours. Immunofluorescence microscopy and Western blot analysis were used to determine the localization and expression of TbetaR-I and -II. Unwounded rat corneas served as control samples. To determine the effect of epidermal growth factor (EGF) and TGF-beta1 on p15(INK4b) and TbetaR-I and -II expression, human corneal epithelial cells were grown in culture to 50% to 60% confluence, and EGF (5 ng/ml) and/or TGF-beta1 (2 ng/ml) were added for 6 hours. Cells were harvested and p15(INK4b) and TBR-I and -II levels were assayed by using Western blot analysis. RESULTS: In unwounded corneas, TbetaR-I and TbetaR-II were present at low levels across the cornea, with higher levels in limbal epithelium. Both TbetaR-I and -II were upregulated after wounding. However, levels of TbetaR-II appeared to increase in the epithelial cells that had migrated to cover the wound area, whereas TbetaR-I was upregulated in the entire corneal epithelium. Western blot analysis indicated that both TbetaR-I and -II were upregulated threefold after wounding. In cultured cells, EGF and TGF-beta1 stimulated TbetaR-II; however, neither one stimulated TbetaR-I expression. TGF-beta1 stimulated p15(INK4b) protein levels threefold. CONCLUSIONS: After wounding, TbetaR-I and TbetaR-II were both expressed at high levels in cells migrating to cover a corneal wound, suggesting that TGF-beta signaling is involved in blocking migrating cells from progressing through the cell cycle. This blockage, at least in part, involves the inhibitor p15(INK4b). In addition, although both TbetaR-I and TbetaR-II are upregulated during wound repair, they appear to be differentially regulated.

Objects referenced in this article

Gene	Tgfbr2	transforming growth factor, beta receptor 2	Rattus norvegicus

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