Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.6.1.3 (ATPase)
 65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The Na+, K+-ATPase pump site density on corneal endothelial cells from Fuchs' endothelial dystrophy corneas has been shown to be drastically decreased in end-stage disease (McCartney et al, Invest Ophthalmol Vis Sci 28:1955, 1987) and significantly increased in the early stages (Geroski et al, Ophthalmology 92:759, 1985) as compared to normal endothelium. In order to provide values for corneas between these two extremes, eye bank corneas from donors with no evidence of corneal edema but with guttata across the extent of the cornea were processed for autoradiography as well as immunohistochemistry. Pump site density was increased compared to end-stage disease but was less than values reported for either functional tissue or early stage disease. Similarly, immunohistochemistry results showed the amount of Na+, K+-ATPase antibody localization to be increased in respect to end-stage disease, but reduced as compared to functional tissue. These results suggest that pump site density on endothelial cells affected with Fuchs' endothelial dystrophy follows a gradual decline towards end-stage disease values as opposed to a sudden sharp deterioration after an initial increase.
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PMID:Moderate Fuchs' endothelial dystrophy ATPase pump site density. 254 44

Proper corneal hydration is maintained by a Na, K-ATPase pump located in the lateral membranes of the endothelial cells. In dysfunctional corneas this pumping action appears to break down as the corneas become edematous. In order to provide quantitative and qualitative data on the Na, K-ATPase pump site density on dysfunctional and functional human corneal endothelial cells, the present study has employed both autoradiographic and histochemical techniques. Computer-assisted morphometrics and statistical analysis showed that there was a significant reduction (P less than 0.001) in 3H-ouabain binding, and thus ATPase pump sites, in the three types of corneas (Fuchs' endothelial dystrophy, aphakic and pseudophakic bullous keratopathy) with dysfunctional endothelia as compared to both types of corneas (eye bank, keratoconus) with functional endothelial cells. There were no significant differences amongst the dysfunctional types or between the two functional types of corneal endothelial cells in respect to density of silver grains. Histochemical staining for ATPase showed less p-nitro-phenylphosphatase histochemical reaction product present on dysfunctional endothelial lateral membranes than in the functional cells.
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PMID:ATPase pump site density in human dysfunctional corneal endothelium. 282 99

Previous light microscopic autoradiographic results from our laboratory have shown a quantitative decrease in ATPase pump site density in dysfunctional corneal endothelium. In order to develop antibody techniques to correlate these findings with electron microscopic localization of pump sites, three types of corneas with dysfunctional endothelium (Fuchs' endothelial dystrophy, aphakic and pseudophakic bullous keratopathy) and two types of corneas with functional endothelium (age matched eye bank and keratoconus) were obtained at the time of transplant surgery. Corneas were fixed, frozen and cryostat sections were incubated in a rabbit kidney ATPase primary antibody followed by incubation in an HRP-labeled secondary antibody. Functional endothelia showed dense antibody labeling along the lateral cell membranes and there was a substantial reduction in labeling along the lateral membranes of dysfunctional endothelia. Positive tissue controls of rabbit kidney showed HRP reaction product in the convoluted tubules. Control tissue, incubated in either non-immune serum or primary antibody preabsorbed with ATPase, confirmed the specificity by having diminished or no reaction product. These results provide immunohistochemical confirmation of our autoradiographic data showing a quantitative reduction in pump site density on dysfunctional corneal endothelium.
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PMID:Immunohistochemical localization of ATPase in human dysfunctional corneal endothelium. 282 61

Previous freeze-fracture results from our laboratory have shown a reduction in a population of intramembrane particles in the lateral endothelial membranes from dysfunctional human corneas. The size range of these intramembrane particles corresponds to that which has previously been reported for the glycoprotein enzyme Na, K-ATPase in enzyme enriched freeze-fractured membranes. In order to investigate glycoconjugate changes potentially related to the particle reduction, wheat germ agglutinin (WGA), which has been shown to bind to the sugar residues in the ATPase subunit, was used to label three types of corneas with dysfunctional endothelial cells (Fuchs' endothelial dystrophy, aphakic and pseudophakic bullous keratopathy) and two types of corneas (eye bank and keratoconus) with functional endothelium using the technique of thin section freeze-fracture label. Apical WGA labelling on all types of dysfunctional cells was shown to be drastically reduced in comparison to both types of functional corneal endothelial cells. Lateral membranes of dysfunctional cells, exposed by freeze-fracturing, also showed a great reduction in WGA labelling as compared to the fractured lateral membranes of functional cells. The differences observed in lectin labelling of lateral membranes may be related in part to the decreased intramembrane particle density observed in dysfunctional human corneal endothelial cells.
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PMID:Freeze-fracture label of functional and dysfunctional human corneal endothelium. 358 77