Localization of thiazide-sensitive Na+-Cl- cotransport and associated geneproducts in mouse DCT

Citation
V. Campean et al., Localization of thiazide-sensitive Na+-Cl- cotransport and associated geneproducts in mouse DCT, AM J P-REN, 281(6), 2001, pp. F1028-F1035
Citations number
29
Language
INGLESE
art.tipo
Article
Categorie Soggetti
da verificare
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY
ISSN journal
0363-6127 → ACNP
Volume
281
Issue
6
Year of publication
2001
Pages
F1028 - F1035
Database
ISI
SICI code
0363-6127(200112)281:6<F1028:LOTNCA>2.0.ZU;2-Y
Abstract
The mammalian distal nephron develops a complex assembly of specialized cel l types to accomplish the fine adjustment of urinary electrolyte compositio n. The epithelia of the distal convoluted tubule (DCT), the connecting tubu le (CNT), and the cortical collecting duct (CCD) show an axial structural h eterogeneity that has been functionally elucidated by the localization of p roteins involved in transepithelial ion transport. We compared the distribu tion of the thiazide-sensitive Na+-Cl- cotransporter (TSC), basolateral Na/Ca2+ exchanger (Na/Ca), cytosolic calcium-binding proteins calbindin D-28K and parvalbumin, and the key enzyme for selective aldosterone actions, 11 beta -hydroxysteroid-dehydrogenase 2 (11HSD2), in the distal convolutions o f the mouse. In the mouse, as opposed to the rat, we found no clear subsegm entation of the DCT into a proximal (DCT1) and a distal (DCT2) portion. The TSC was expressed along the entire DCT. Na/Ca and calbindin D28K were simi larly expressed along most of the DCT, with minor exceptions in the initial portion of the DCT. Both were also present in the CNT. Parvalbumin was fou nd in the entire DCT, with an occasional absence from short end portions of the DCT, and was not present in CNT. 11HSD2 was predominantly located in t he CNT and CCD. Short end portions of DCT only occasionally showed the 11HS D2 signal. We also observed an overlap of 11HSD2 immunoreactivity and mRNA staining. Our observations will have implications in understanding the phys iological effects of gene disruption and targeting experiments in the mouse .