May 2003
Volume 44, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2003
Galectins-3 and -7 Play a Role in Re-epithelialization of Corneal Wounds
Author Affiliations & Notes
  • Z. Cao
    Ophthalmology, New England Eye Center & Center for Vision Research, Tufts University, Boston, MA, United States
  • N. Said
    Ophthalmology, New England Eye Center & Center for Vision Research, Tufts University, Boston, MA, United States
  • M. Garate
    Ophthalmology, New England Eye Center & Center for Vision Research, Tufts University, Boston, MA, United States
  • F. Liu
    Dermatology, UC Davis, Davis, CA, United States
  • N. Panjwani
    Dermatology, UC Davis, Davis, CA, United States
  • Footnotes
    Commercial Relationships  Z. Cao, None; N. Said, None; M. Garate, None; F. Liu, None; N. Panjwani, None.
  • Footnotes
    Support  NIH Grant EY07088 and EY09340; EYP3013078
Investigative Ophthalmology & Visual Science May 2003, Vol.44, 3827. doi:
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      Z. Cao, N. Said, M. Garate, F. Liu, N. Panjwani; Galectins-3 and -7 Play a Role in Re-epithelialization of Corneal Wounds . Invest. Ophthalmol. Vis. Sci. 2003;44(13):3827.

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

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Abstract

Abstract: : Purpose: Disorders of corneal wound healing characterized by impaired or delayed re-epithelialization are a serious medical problem. Recent studies from our laboratory have suggested that a carbohydrate-binding protein, galectin-3, plays a role in re-epithelialization of corneal wounds. We have shown that the rate of re-epithelialization of corneal wound is perturbed in galectin-3-deficient (gal3-/-) mice and that the exogenous galectin-3 stimulates re-epithelialization of corneal wounds in gal3+/+ mice. The goal of the present study was to characterize the molecular mechanism by which galectin-3 modulates re-epithelialization of corneal wounds. Methods: BrdU in vivo labeling was used to determine whether the rate of corneal epithelial cell proliferation is perturbed in gal3-/- mice. In vitro experiments were performed to determine whether the exogenous galectin-3 stimulates re-epithelialization of corneal wounds in gal3-/- mice. Gene expression patterns of healing gal3+/+ and gal3-/- mice were compared using cDNA microarrays. Results: Quantitation of the BrdU-labeled cells in gal3+/+ and gal3-/- corneas revealed that corneal epithelial cell proliferation rate is not perturbed in gal3-/- corneas. Exogenous galectin-3 accelerated re-epithelialization of wounds in gal3+/+ mice but, surprisingly, not in the gal3-/- mice. Gene expression analysis using cDNA microarrays revealed that healing corneas of gal3-/- mice contain markedly reduced levels of another carbohydrate-binding protein, galectin-7, compared to those of gal3+/+ mice. More importantly, unlike galectin-3, galectin-7 accelerated re-epithelialization of wounds in both gal3-/- and gal3+/+ mice. The stimulatory effect was specifically inhibited by a competing disaccharide, ß-lactose. Conclusions: These findings lead us to propose that galectins-3 and –7 bind to distinct counterreceptors and that the corneas of gal3-/- mice may be deficient in the expression of the counterreceptors of the lectin itself. We further propose that galectin-3 may in fact modulate the expression of glycosyltransferases, which in turn, regulate glycosylation of the proteins which serve as cell surface or ECM counterreceptors of the lectin. Alternatively, galectin-3 may influence re-epithelialization of corneal wounds by modulating the expression of galectin-7. Regardless of the mechanisms involved, our findings that both galectins-3 and -7 stimulate re-epithelialization of corneal wounds have broad implications for developing novel therapeutic strategies for the treatment of nonhealing wounds.

Keywords: cornea: epithelium • wound healing • cell adhesions/cell junctions 
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