IOVS Learning & Memory
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Sasaki, Y.
Right arrow Articles by McLaughlin, B. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Sasaki, Y.
Right arrow Articles by McLaughlin, B. J.

Investigative Ophthalmology & Visual Science, Vol 27, 480-485, Copyright © 1986 by Association for Research in Vision and Ophthalmology


ARTICLES AND REPORTS

Freeze fracture study of human corneal endothelial dysfunction

Y Sasaki, AW Tuberville, TO Wood and BJ McLaughlin

Intramembrane changes occurring in dysfunctional corneal endothelial cell membranes were examined using freeze-fracture and transmission electron microscopy techniques. Three categories of dysfunctional endothelium were examined: aphakic bullous keratopathy, pseudophakic bullous keratopathy and Fuchs' endothelial dystrophy. Keratoconus corneas and a donor eye bank eye were examined as normal controls. Four intramembrane changes were observed on replicas of freeze-fractured membranes in each category of dysfunctional endothelium. These were a marked reduction in intramembrane particle density on lateral membranes, altered apico-lateral junctional complexes, increased vesicle fusion sites on apical, lateral and basal membranes, and abnormal desmosome-like particle aggregates on the lateral endothelial cell membranes. The marked reduction in intramembrane particles on lateral membranes may be due to a change in the macromolecular components associated with pump dysfunction. The increase in membrane vesicle fusion sites and the breakdown in intercellular junctions may be associated with increased permeability during barrier dysfunction.


This article has been cited by other articles:


Home page
J. Histochem. Cytochem.Home page
M. C. Kenney, S. R. Atilano, N. Zorapapel, B. Holguin, R. N. Gaster, and A. V. Ljubimov
Altered Expression of Aquaporins in Bullous Keratopathy and Fuchs' Dystrophy Corneas
J. Histochem. Cytochem., October 1, 2004; 52(10): 1341 - 1350.
[Abstract] [Full Text] [PDF]


Home page
J. Histochem. Cytochem.Home page
A. V. Ljubimov, M. Saghizadeh, R. Pytela, D. Sheppard, and M. C. Kenney
Increased Expression of Tenascin-C-binding Epithelial Integrins in Human Bullous Keratopathy Corneas
J. Histochem. Cytochem., November 1, 2001; 49(11): 1341 - 1350.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1986 by the Association for Research in Vision and Ophthalmology