May 2008
Volume 49, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2008
The Role of Thrombospondin-1 in Rat Corneal Wound Healing
Author Affiliations & Notes
  • M. Matsuba
    Schepens Eye Research Institute, Boston, Massachusetts
    Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts
  • A. E. K. Hutcheon
    Schepens Eye Research Institute, Boston, Massachusetts
    Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts
  • J. D. Zieske
    Schepens Eye Research Institute, Boston, Massachusetts
    Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts
  • Footnotes
    Commercial Relationships  M. Matsuba, None; A.E.K. Hutcheon, None; J.D. Zieske, None.
  • Footnotes
    Support  NIH Grant EY05665
Investigative Ophthalmology & Visual Science May 2008, Vol.49, 2964. doi:
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    • Get Citation

      M. Matsuba, A. E. K. Hutcheon, J. D. Zieske; The Role of Thrombospondin-1 in Rat Corneal Wound Healing. Invest. Ophthalmol. Vis. Sci. 2008;49(13):2964.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: : Recent studies have indicated that thrombospondin-1 (TSP-1) can activate the latent complex of transforming growth factor-β (TGF-β). TGF-β has been shown to play a major role in stimulating mesenchymal cells to synthesize extra-cellular matrix. After corneal injury, keratocytes become active and transform into corneal fibroblasts or myofibroblasts. It is our purpose to determine if TSP-1 regulates the transformation of keratocytes into myofibroblasts (MF) via TGF-β. In this study, we investigated the expression of TSP-1 and α-smooth muscle actin (α-SMA), a marker of MF, in a superficial keratectomy wound model.

Methods: : A 3-mm superficial keratectomy wound was made in central rat corneas and allowed to heal 8 hours to 2 weeks in vivo. Unwounded normal eyes served as controls. Expression of TSP-1, Ki67 and α-SMA was examined by indirect immunofluorescence microscopy.

Results: : In unwounded corneas, TSP-1 expression was observed primarily in the endothelium, Ki67 was localized in the epithelial basal cells and no α-SMA was present in the central cornea. By 48 hours, TSP-1 expression appeared in the wounded stroma immediately subjacent to the wound-healing epithelium, and Ki67 was present in the stromal cells peripheral to the wound area. However, α-SMA-expressing cells were not observed in the wound area until 3-4 days after wounding. When they were observed, they were within the same area that TSP-1 was localized. At 1 week, the expression of α-SMA and TSP-1 appeared to peak. This expression seemed to decrease by 2 weeks. There was no apparent correlation between the expression of Ki67 and either TSP-1 or α-SMA. The expression of myofibroblasts in the wounded stroma was confirmed by electron microscopy.

Conclusions: : TSP-1 may play a key role during corneal stromal repair by inducing myofibroblast generation. In our future studies, we will examine the correlation between TSP-1, TGF-β and α-SMA by immunoblotting, and will focus on determining which cells express TSP-1.

Keywords: growth factors/growth factor receptors • cornea: stroma and keratocytes • wound healing 
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