| TGF-beta receptor types I and II are differentially expressed during corneal epithelial wound repair. | |
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MedLine Citation:
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PMID: 11381048 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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PURPOSE: It has been demonstrated that cells migrating to cover an epithelial débridement 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 débridement 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. |
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Authors:
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J D Zieske; A E Hutcheon; X Guo; E H Chung; N C Joyce |
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Publication Detail:
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Type: Journal Article; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Investigative ophthalmology & visual science Volume: 42 ISSN: 0146-0404 ISO Abbreviation: Invest. Ophthalmol. Vis. Sci. Publication Date: 2001 Jun |
Date Detail:
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Created Date: 2001-05-30 Completed Date: 2001-06-28 Revised Date: 2009-11-19 |
Medline Journal Info:
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Nlm Unique ID: 7703701 Medline TA: Invest Ophthalmol Vis Sci Country: United States |
Other Details:
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Languages: eng Pagination: 1465-71 Citation Subset: IM |
Affiliation:
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Schepens Eye Research Institute and Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts 02114-2500, USA. zieske@vision.eri.harvard.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Activin Receptors, Type I* Animals Blotting, Western Cell Culture Techniques / methods Epithelium, Corneal / injuries, metabolism* Female Fluorescent Antibody Technique, Indirect Male Protein-Serine-Threonine Kinases / metabolism* Rats Rats, Sprague-Dawley Receptors, Transforming Growth Factor beta / metabolism* Up-Regulation Wound Healing* |
| Grant Support | |
ID/Acronym/Agency:
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R01 EY05665/EY/NEI NIH HHS; R01 EY05767/EY/NEI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Receptors, Transforming Growth Factor beta; EC 2.7.1.11/TGF-beta type I receptor; EC 2.7.11.1/Protein-Serine-Threonine Kinases; EC 2.7.11.30/Activin Receptors, Type I; EC 2.7.11.30/transforming growth factor-beta type II receptor |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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