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Sodium retention in rats with liver cirrhosis is associated with increased renal abundance of NaCl cotransporter (NCC)


Yu, Zhenrong; Serra, Andreas; Sauter, Daniel; Loffing, Johannes; Ackermann, Daniel; Frey, Felix J; Frey, Brigitte M; Vogt, Bruno (2005). Sodium retention in rats with liver cirrhosis is associated with increased renal abundance of NaCl cotransporter (NCC). Nephrology, Dialysis, Transplantation, 20(9):1833-1841.

Abstract

Background. Liver cirrhosis is associated with enhanced renal tubular sodium retention, the mechanism of which is still debated. We hypothesized that liver cirrhosis is associated with increased expression of renal epithelial sodium transporter(s). Methods. Liver cirrhosis was induced by bile duct ligation (BDL) in rats. Steady state mRNA of ENaC subunits α, β, γ serum and glucocorticoid inducible kinase (Sgk1) were measured by TaqMan PCR in kidney homogenates at week 1, 2, 3 and 4 after BDL. Renal protein content of ENaC subunits, ubiquitin-protein-ligase Nedd4-2 and NaCl cotransporter (NCC) were assessed by western blot. Subcellular localization of ENaC subunits and NCC were analysed by immunohistochemistry. Results. Steady state mRNA of ENaC α, β and γ were unchanged during the 4 weeks investigated, while ENaC protein decreased most prominently at week 2 (control vs BDL; α, −46%; β, −81%; and γ, −63%; n = 6). Subcellular localization of ENaC subunits was not altered at week 2. Sgk1 mRNA did not change, whereas Nedd4-2 protein was reduced by >50% 2-4 weeks after BDL. NCC protein significantly increased at week 1 (control vs BDL: +66%, n = 6, P<0.05) and decreased at week 3 (control vs BDL: −85%, n = 6, P<0.0005). Conclusions. Enhanced abundance of NCC was observed in the initial stage after BDL, followed by a marked decrease. ENaC transcription, translation or cell surface abundance was not increased after BDL

Abstract

Background. Liver cirrhosis is associated with enhanced renal tubular sodium retention, the mechanism of which is still debated. We hypothesized that liver cirrhosis is associated with increased expression of renal epithelial sodium transporter(s). Methods. Liver cirrhosis was induced by bile duct ligation (BDL) in rats. Steady state mRNA of ENaC subunits α, β, γ serum and glucocorticoid inducible kinase (Sgk1) were measured by TaqMan PCR in kidney homogenates at week 1, 2, 3 and 4 after BDL. Renal protein content of ENaC subunits, ubiquitin-protein-ligase Nedd4-2 and NaCl cotransporter (NCC) were assessed by western blot. Subcellular localization of ENaC subunits and NCC were analysed by immunohistochemistry. Results. Steady state mRNA of ENaC α, β and γ were unchanged during the 4 weeks investigated, while ENaC protein decreased most prominently at week 2 (control vs BDL; α, −46%; β, −81%; and γ, −63%; n = 6). Subcellular localization of ENaC subunits was not altered at week 2. Sgk1 mRNA did not change, whereas Nedd4-2 protein was reduced by >50% 2-4 weeks after BDL. NCC protein significantly increased at week 1 (control vs BDL: +66%, n = 6, P<0.05) and decreased at week 3 (control vs BDL: −85%, n = 6, P<0.0005). Conclusions. Enhanced abundance of NCC was observed in the initial stage after BDL, followed by a marked decrease. ENaC transcription, translation or cell surface abundance was not increased after BDL

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Item Type:Journal Article, refereed, original work
Communities & Collections:National licences > 142-005
Dewey Decimal Classification:570 Life sciences; biology
Scopus Subject Areas:Health Sciences > Nephrology
Health Sciences > Transplantation
Language:English
Date:1 September 2005
Deposited On:23 Oct 2018 09:50
Last Modified:09 Apr 2020 00:15
Publisher:Oxford University Press
ISSN:0931-0509
OA Status:Green
Free access at:Publisher DOI. An embargo period may apply.
Publisher DOI:https://doi.org/10.1093/ndt/gfh916
Related URLs:https://www.swissbib.ch/Search/Results?lookfor=nationallicenceoxford101093ndtgfh916 (Library Catalogue)

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