May 2005
Volume 46, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2005
Expression of Junctional Adhesion Molecules, JAM–1, JAM–2, JAM–3 in Normal and Inflamed Human Corneas
Author Affiliations & Notes
  • W.E. Philipp
    Dept Ophthalmology, Medical University Innsbruck, Innsbruck, Austria
  • L.E. Speicher
    Dept Ophthalmology, Medical University Innsbruck, Innsbruck, Austria
  • Footnotes
    Commercial Relationships  W.E. Philipp, None; L.E. Speicher, None.
  • Footnotes
    Support  None.
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 2637. doi:
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      W.E. Philipp, L.E. Speicher; Expression of Junctional Adhesion Molecules, JAM–1, JAM–2, JAM–3 in Normal and Inflamed Human Corneas . Invest. Ophthalmol. Vis. Sci. 2005;46(13):2637.

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Abstract

Abstract: : Purpose: Junctional adhesion molecules, JAM–1, JAM–2, JAM–3 are novel transmembrane proteins of tight junctions which are required for the regulation of the paracellular permeability across epithelial and endothelial cells. Furthermore, these adhesion molecules were recently shown to be involved in the adhesion and particularly in the transmigration (diapedesis) of monocytes, neutrophils and lymphocytes across the vessel wall during inflammation. In addition, JAM–1 was demonstrated to play an essential role in basic fibroblast growth factor–induced angiogenesis. The aim of the present study was to investigate whether JAM–1, JAM–2, JAM–3 are expressed in normal and inflamed human corneas to shed more light on the role of these adhesion molecules in leukocyte trafficking, inflammation and angiogenesis in the cornea. Methods: Immunohistochemistry was performed using the streptavidin–biotin–peroxidase method and highly specific antibodies against JAM–1, JAM–2 and JAM–3 in 5 normal human corneas with a scleral rim from human donor eyes and in 18 vascularized human corneas obtained at the time of penetrating keratoplasty in patients with various corneal diseases. Results: In normal corneas JAM–1 and JAM–2 were expressed on corneal epithelial cells and on endothelial cells of limbal vessels while JAM–3 was expressed on keratocytes in the stroma, on endothelial cells of limbal vessels and on corneal endothelial cells. In inflamed and vascularized corneas positive immunostaining of JAM–1, JAM–2 and JAM–3 was also found on vascular endothelial cells of newly formed vessels in the stroma. In addition, JAM–3 expression was increased on keratocytes/fibroblasts in the stroma particularly at sites of scar tissue or inflammation. Conclusions: The results of the present study demonstrate that JAM–1, JAM–2 and JAM–3 are expressed in normal and inflamed human corneas. The expression of these junctional adhesion molecules on endothelial cells of limbal vessels and on newly formed vessels in the stroma of inflamed corneas suggest that these molecules may be involved in the sequential steps of leukocyte transmigration and recruitment to sites of inflammation and in the pathogenesis of neovascularization in various inflammatory corneal diseases.

Keywords: cornea: basic science • inflammation • neovascularization 
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