March 1997
Volume 38, Issue 3
Free
Articles  |   March 1997
Detection of cell adhesion molecules in lens epithelial cells of human cataracts.
Author Affiliations
  • O Nishi
    Nishi Eye Hospital, Osaka, Japan.
  • K Nishi
    Nishi Eye Hospital, Osaka, Japan.
  • T Akaishi
    Nishi Eye Hospital, Osaka, Japan.
  • E Shirasawa
    Nishi Eye Hospital, Osaka, Japan.
Investigative Ophthalmology & Visual Science March 1997, Vol.38, 579-585. doi:
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      O Nishi, K Nishi, T Akaishi, E Shirasawa; Detection of cell adhesion molecules in lens epithelial cells of human cataracts.. Invest. Ophthalmol. Vis. Sci. 1997;38(3):579-585.

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

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Abstract

PURPOSE: To detect the expression of cell adhesion molecules (CAMs), including beta integrins, intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1, leukocyte-endothelial cell adhesion molecule-2, E-cadherin, and CD44, in cultured lens epithelial cells (LECs) of human cataracts. To show that LECs attach to cells or extracellular matrix components by the detected adhesion molecules. METHODS: A circular section of the anterior capsule with attached LECs obtained by anterior capsulotomy during cataract surgery was cultured in a well of an eight-chamber slide. The LEC immediately after surgery and the cell outgrowth beyond the capsular margin at 2 weeks of culture were observed after the culture was stained immunohistochemically. Functional assays of LEC growth on collagen- or laminin-coated plates were performed in the presence and absence of the antibody blocking the detected adhesion molecules. RESULTS: beta 1 integrin, ICAM-1, and CD44 were detected in both the original specimens and the cultured cells. When the antihuman anti-beta 1 integrin monoclonal antibody (mAb), anti-ICAM-1 mAb, or anti-CD44 mAb was added at 10 micrograms/ml to the incubation medium, LEC migration and proliferation were inhibited significantly on the collagen- or laminin-coated plates. When the mAb blocking these three CAMs were added each at 1 microgram/ml, LEC proliferation also were inhibited. CONCLUSIONS: beta 1 integrin, ICAM-1 and CD44 are all involved in LEC attachment and growth on collagen and laminin in vitro. It can be assumed that these CAMs are involved in adhesion of LECs to extracellular matrix components of the lens capsule. Understanding the characteristics of the adhesion molecules in LEC may lead to the development of a new approach to inhibit secondary cataract formation.

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