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Fig. 4. Differentiation of the TAL, MD and DCT was impaired in the
Brn1-deficient kidney. (A) In situ hybridization analyses of the TAL
in newborn Brn1+/+ and Brn1-/-
kidneys. The expression of the Tamm-Horsfall glycoprotein gene
(Umod), the prostaglandin E2 receptor subtype
EP3 gene (Ptger3) and bumetanide-sensitive Na-K- 2Cl
co-transporter gene (Nkcc2/Slc12a1) was detected in the TAL of the
Brn1+/+, but not the Brn1-/- kidney,
suggesting that TAL differentiation was impaired in Brn1-deficient animals.
Scale bar: 50 µm. (B) Histological and in situ hybridization analyses of
the MD and the surrounding TAL cells in Brn1+/+ and
Brn1-/- kidneys. PAS staining demonstrates that the MD in
Brn1+/+ kidneys (arrows) possesses the defining MD
features; cells are crowded and protrude into the tubular lumen. The putative
MD in Brn1-/- mice (arrowheads) does not display these
features. Using in situ hybridization analysis, expression of the constitutive
type 1 isoform of nitric oxide synthase gene (Nos1) was detected in
the MD of the Brn1+/+, but not the
Brn1-/- kidney. Ptger3 expression was detected in
both the MD and the surrounding TAL cells of Brn1+/+
kidney but was absent from the Brn1-/- kidney. Scale bar:
20 µm. (C) In situ hybridization analysis of DCT in
Brn1+/+ and Brn1-/- kidneys. The
expression of the thiazide-sensitive Na-Cl co-transporter gene
(Ncc/Slc12a3), a maker for DCT, was detected in
Brn1+/+ but not Brn1-/- kidneys. The
expression of the Na/Ca exchanger gene (Ncx1/Slc8a1), a maker of the
distal part of the DCT and for the CNT, was altered in
Brn1-/- kidneys in comparison with that of
Brn1+/+ kidneys, suggesting that Ncx1 expression
in Brn1-/- kidneys remained only in the CNT. The
expression of the amirolide-sensitive epithelial Na+ channel gene
(ßEnaC/Scnn1b), a marker for CNT and CD, was indistinguishable
in Brn1+/+ kidney from that in Brn1-/-
kidneys. Scale bars: 20 µm.
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