RENAL TUBULE NA,K-ATPASE POLARITY IN DIFFERENT ANIMAL-MODELS OF POLYCYSTIC KIDNEY-DISEASE

Citation
Mr. Ogborn et al., RENAL TUBULE NA,K-ATPASE POLARITY IN DIFFERENT ANIMAL-MODELS OF POLYCYSTIC KIDNEY-DISEASE, The Journal of histochemistry and cytochemistry, 43(8), 1995, pp. 785-790
Citations number
21
Categorie Soggetti
Cell Biology
ISSN journal
00221554
Volume
43
Issue
8
Year of publication
1995
Pages
785 - 790
Database
ISI
SICI code
0022-1554(1995)43:8<785:RTNPID>2.0.ZU;2-K
Abstract
Apical mislocation of the ubiquitous transport enzyme Na,K-ATPase has been implicated as a feature of cyst development in in vitro studies o f human polycystic kidney disease (PKD) epithelia. We undertook an imm unohistochemical study of murine glucocorticoid-induced PKD, the peg m ouse, the cpk mouse, and the diphenylthiazole (DPT)-induced rat models of PKD to determine if this feature was common to these models of cys t development, Distribution of Na,K-ATPase was determined with a polyc lonal anti-Na,K-ATPase antibody and a nickel-silver-enhanced peroxidas e color development system, Results were documented objectively with d ensitometric techniques, Control animals appropriate to the age, strai n, and species of the experimental groups demonstrated the expected po lar distribution of Na,K-ATPase to the basolateral surface, This distr ibution was more marked in mature animals, Tubular dilatation and cyst ic change, however, were associated with increased apical Na,K-ATPase in all models. The murine models demonstrated decreased basolateral st aining for Na,K-ATPase compared with controls, although this was not a feature of the DPT rat model, Abnormal location of Na,K-ATPase is a s hared feature of a variety of animal models and human PKD. This may co ntribute to abnormal fluid and electrolyte flux favoring cyst formatio n or may represent expression of a less differentiated renal tubule ep ithelial phenotype.