May 1996
Volume 37, Issue 6
Free
Articles  |   May 1996
Extracellular matrix alterations in human corneas with bullous keratopathy.
Author Affiliations
  • A V Ljubimov
    Ophthalmology Research Laboratories, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
  • R E Burgeson
    Ophthalmology Research Laboratories, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
  • R J Butkowski
    Ophthalmology Research Laboratories, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
  • J R Couchman
    Ophthalmology Research Laboratories, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
  • R R Wu
    Ophthalmology Research Laboratories, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
  • Y Ninomiya
    Ophthalmology Research Laboratories, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
  • Y Sado
    Ophthalmology Research Laboratories, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
  • E Maguen
    Ophthalmology Research Laboratories, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
  • A B Nesburn
    Ophthalmology Research Laboratories, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
  • M C Kenney
    Ophthalmology Research Laboratories, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
Investigative Ophthalmology & Visual Science May 1996, Vol.37, 997-1007. doi:
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    • Get Citation

      A V Ljubimov, R E Burgeson, R J Butkowski, J R Couchman, R R Wu, Y Ninomiya, Y Sado, E Maguen, A B Nesburn, M C Kenney; Extracellular matrix alterations in human corneas with bullous keratopathy.. Invest. Ophthalmol. Vis. Sci. 1996;37(6):997-1007.

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

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Abstract

PURPOSE: To uncover abnormalities of extracellular matrix (ECM) distribution in human corneas with pseudophakic and aphakic bullous keratopathy (PBK/ABK). METHODS: Indirect immunofluorescence with antibodies to 27 ECM components was used on frozen sections of 14 normal and 20 PBK/ABK corneas. RESULTS: Fibrillar deposits of an antiadhesive glycoprotein tenascin in the anterior and posterior stroma, epithelial basement membrane (BM), bullae and subepithelial fibrosis (SEF) areas, and posterior collagenous layer (PCL) were revealed in disease corneas. Tenascin in midstroma, which was observed in some cases, correlated with decreased visual acuity. In normal central corneas, tenascin was never found. Other major ECM abnormalities in PBK/ABK corneas compared to normals included: discontinuous epithelial BM straining for laminin-1 (alpha 1 beta 1 gamma 1), entactin/nidogen and fibronectin; accumulation of fibronectin and alpha 1-alpha 2 type IV collagen on the endothelial face of the Descemet's membrane; and abnormal deposition of stromal ECM (tenascin, fibronectin, decorin, types I, III, V, VI, VIII, XII, XIV collagen) and BM components (type IV, collagen, perlecan, bamacan, laminin-1, entactin-nidogen, fibronectin) in SEF areas and in PCL. CONCLUSIONS: The study provides a molecular description of an ongoing fibrosis on the epithelial, stomal, and endothelial levels in PBK/ABK corneas. These fibrotic changes may follow initial endothelial damage after cataract surgery, may be caused by the upregulation of fibrogenic cytokines, and may play a significant role in the progression of bullous keratopathy.

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