Sodium pump distribution is not reversed in the DBA/2FG-pcy, polycystic kidney disease model mouse.
Recently, it has been reported that Na,K-ATPase in the renal epithelia of human autosomal dominant polycystic kidney disease and cpk mouse, a murine model of autosomal recessive polycystic kidney disease, mislocates to apical plasma membrane and that mislocated Na,K-ATPase causes the cyst formation. Whether the DBA/2FG-pcy mice, which are presumably a suitable model for autosomal dominant polycystic kidney disease, also exhibit the reversal polarity of Na,K-ATPase localization was examined. Kidneys of newborn DBA/2FG-pcy mice, and those at early and late stages of cyst development were examined by immunohistochemical techniques. At any stage, abnormal distribution of Na,K-ATPase on the apical membranes of tubular epithelial cells could not be detected. It is suggested that cysts can be formed without reversed polarity of Na,K-ATPase distribution in pcy mice.
Kawa
G
G
Department of Urology, Kansai Medical University, Osaka, Japan.
Nagao
S
S
Yamamoto
A
A
Omori
K
K
Komatz
Y
Y
Takahashi
H
H
Tashiro
Y
Y
D000818:Animals; D000831:Animals, Newborn; D015153:Blotting, Western; D004195:Disease Models, Animal; D018450:Disease Progression; D004848:Epithelium / Q000201:enzymology; D006801:Humans; D007124:Immunoenzyme Techniques; D007150:Immunohistochemistry; D007668:Kidney / Q000201:enzymology* / Q000648:ultrastructure; D051379:Mice; D008811:Mice, Inbred DBA; D008817:Mice, Mutant Strains / Q000235:genetics / Q000378:metabolism*; D016891:Polycystic Kidney, Autosomal Dominant / Q000201:enzymology* / Q000235:genetics; D016622:Silver Staining; D000254:Sodium-Potassium-Exchanging ATPase / Q000032:analysis* / Q000378:metabolism*
D000254:Sodium-Potassium-Exchanging ATPase