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ATPase pump site density in human dysfunctional corneal endothelium
M D McCartney1, D P Robertson, T O Wood
1Department of Anatomy, College of Medicine, University of Tennessee at Memphis 38163.
Investigative Ophthalmology & Visual Science
|December 1, 1987
Summary
Human corneal endothelial cells with dysfunctional corneas show a significant reduction in sodium-potassium adenosine triphosphatase (Na, K-ATPase) pump sites. This finding helps explain corneal edema in certain eye conditions.
Area of Science:
- Ophthalmology
- Cell Biology
- Biochemistry
Background:
- Corneal hydration is crucial for vision and is maintained by Na, K-ATPase pumps in endothelial cells.
- Dysfunctional corneas often exhibit edema, suggesting a breakdown in endothelial pump activity.
Purpose of the Study:
- To quantitatively and qualitatively assess Na, K-ATPase pump site density in human corneal endothelial cells.
- To compare pump site density between dysfunctional and functional corneal endothelium.
Main Methods:
- Autoradiographic techniques using 3H-ouabain binding.
- Histochemical staining for ATPase activity.
- Computer-assisted morphometrics and statistical analysis.
Main Results:
- A significant reduction (P < 0.001) in 3H-ouabain binding, indicating fewer ATPase pump sites, was observed in dysfunctional corneas (Fuchs' dystrophy, bullous keratopathy) compared to functional corneas (eye bank, keratoconus).
- No significant differences in pump site density were found among the dysfunctional types or between the functional types.
- Histochemical staining revealed less ATPase reaction product on the lateral membranes of dysfunctional endothelial cells.
Conclusions:
- Human corneal endothelial cells in dysfunctional corneas have a significantly reduced density of Na, K-ATPase pump sites.
- This reduction in pump sites likely contributes to the development of corneal edema.
- The findings provide quantitative evidence for endothelial dysfunction at the molecular level.