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
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.