December 1993
Volume 34, Issue 13
Free
Articles  |   December 1993
Apolipoprotein A-I and B distribution in the human cornea.
Author Affiliations
  • F Ashraf
    Clinical Branch, National Eye Institute, National Institutes of Health, Bethesda, MD 20892.
  • D G Cogan
    Clinical Branch, National Eye Institute, National Institutes of Health, Bethesda, MD 20892.
  • H S Kruth
    Clinical Branch, National Eye Institute, National Institutes of Health, Bethesda, MD 20892.
Investigative Ophthalmology & Visual Science December 1993, Vol.34, 3574-3578. doi:
  • Views
  • PDF
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      F Ashraf, D G Cogan, H S Kruth; Apolipoprotein A-I and B distribution in the human cornea.. Invest. Ophthalmol. Vis. Sci. 1993;34(13):3574-3578.

      Download citation file:


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

      ×
  • Supplements
Abstract

PURPOSE: To determine the presence and localization of apolipoprotein A-I, a marker for high density lipoprotein, and apolipoprotein B, a marker for low density lipoprotein, in human cornea; to examine the relationship of these lipoprotein markers with areas of lipid accumulation in the cornea. METHODS: A-I and B apolipoproteins were localized in frozen sections of human corneas with specific monoclonal antibodies using avidin-biotin immunoperoxidase labelling. Corneal lipid was colocalized with apolipoproteins by oil red 0 staining of immunostained sections. RESULTS: Staining data showed that apolipoprotein B and lipid accumulated in the extracellular spaces of peripheral corneal stroma. However, their distributions were not coincident. The posterior region of peripheral corneal stroma (including Descemet's membrane) often contained lipid without immunodetectable apolipoprotein B. Unexpectedly, apolipoprotein A-I was associated with many keratocytes throughout the cornea in addition to an extracellular distribution heaviest in peripheral cornea. CONCLUSIONS: Lipid deposits lacking apolipoprotein B in peripheral cornea suggest that if accumulated corneal arcus lipid is derived from extracellular deposition of plasma low density lipoprotein, the low density lipoprotein is altered such that it looses its immunoreactive apolipoprotein B. The unexpected association of apolipoprotein A-I with keratocytes suggests that these cells are either taking up or synthesizing a protein sharing an immunoreactive epitope with apolipoprotein A-I.

×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×