Regulation of epithelial sodium channel in puromycin aminonucleoside-induced unilateral experimental nephrotic syndrome in normal and analbuminemic Nagase rats

Détails

ID Serval
serval:BIB_330B77B28A91
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Regulation of epithelial sodium channel in puromycin aminonucleoside-induced unilateral experimental nephrotic syndrome in normal and analbuminemic Nagase rats
Périodique
Nephron. Physiology
Auteur⸱e⸱s
Yu  Z., Schumacher  M., Frey  B. M., Frey  F. J., Vogt  B.
ISSN
1660-2137 (Electronic)
Statut éditorial
Publié
Date de publication
2005
Volume
101
Numéro
3
Pages
P51-P62
Notes
Journal Article
Résumé
BACKGROUND: Nephrotic syndrome (NS) is characterized by renal sodium retention and edema formation. In nephrotic rats the site of enhanced sodium retention has been localized in the cortical collecting duct (CCD). The epithelial sodium channel (ENaC) is the rate-limiting constituent of sodium transport in CCD. Amiloride, an ENaC-blocking drug, corrects the abnormal rate of sodium transport in isolated perfused CCD from puromycin aminonucleoside (PAN)-treated rats. Therefore, we hypothesized that ENaC functional expression is increased in NS. METHODS: Unilateral NS was induced by PAN in Wistar rats and analbuminemic Nagase rats (NAR). Urinary protein excretion, renal abundance of mRNA and protein of ENaC subunits, as well as the ENaC regulatory serum glucocorticoid-inducible kinase (Sgk1) and Nedd4-2, were assessed. RESULTS: Proteinuria appeared at day 2 in the Wistar rats and NAR. Surprisingly a downregulation rather than the expected upregulation of alpha-, beta- and gamma-ENaC mRNA abundance was observed in both Wistar rats and NAR, when the treated kidney was compared with the untreated kidney. The amount of protein of alpha-, beta- and gamma-ENaC was not affected by the NS. Sgk1 mRNA expression did not change and Nedd4-2 protein expression was only decreased at days 1 and 2 in Wistar rats. CONCLUSION: ENaC mRNA and protein expression are not increased in the early phase of unilateral PAN-induced NS. Sgk1, Nedd4-2 and analbuminemia are not important regulatory factors of ENaC protein expression in experimental NS.
Mots-clé
Acetylglucosaminidase/*genetics Animals Antibiotics, Antineoplastic Creatine/urine Epithelial Sodium Channel Immediate-Early Proteins/genetics Male Nephrotic Syndrome/chemically induced/*metabolism/*physiopathology Protein-Serine-Threonine Kinases/genetics Proteinuria/chemically induced/metabolism/physiopathology Puromycin Aminonucleoside RNA, Messenger/analysis Rats Rats, Mutant Strains Rats, Wistar Serum Albumin Sodium/urine Sodium Channels/genetics/*metabolism Ubiquitin-Protein Ligases/metabolism
Pubmed
Création de la notice
25/01/2008 13:03
Dernière modification de la notice
20/08/2019 13:18
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