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Renal epithelial Na channel protein expression is reduced in H,K‐ATPase knockout mice
Author(s) -
Greenlee Megan Michelle,
Lynch I. Jeanette,
Gumz Michelle L.,
Cain Brian D.,
Wingo Charles S.
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.611.15
Subject(s) - epithelial sodium channel , reabsorption , medicine , renal sodium reabsorption , endocrinology , chemistry , messenger rna , knockout mouse , kidney , microbiology and biotechnology , biology , sodium , gene , receptor , biochemistry , organic chemistry
The importance of the epithelial Na + channel (ENaC) to Na + reabsorption is highlighted by genetic gain of function mutations in ENaC that lead to severe hypertension (Liddle's Syndrome). Spicer et al (Am J Phys, 2001) demonstrated that colonic ENaC activity was reduced in HKα 2 −/− mice, suggesting that H + ,K + ‐ATPases are required for complete ENaC function. Given the importance of functional ENaC to renal Na + transport, we investigated whether double knockout of H + ,K + ‐ATPase α subunits in mice (HKα 1,2 −/− ) affected ENaC expression. Real time quantitative PCR was used to evaluate the mRNA expression of α‐, β‐, and γ‐ENaC subunits in cortex and medulla from wild type (WT) and HKα 1,2 −/− mice. Cortical α‐ and β‐ENaC mRNA expression was slightly decreased (~20–25%) in HKα 1,2 −/− mice compared to WT (p=0.10 and 0.08, respectively). Importantly, we observed a 45% reduction in medullary α‐ENaC protein expression (n=3, p<0.05) in HKα 1,2 −/− mice vs WT, as determined by densitometry of immunoblots. In summary, these data suggest that renal H + ,K + ‐ATPases are needed for appropriate expression of ENaC subunits and are important for renal Na + adaptation. Studies were funded by NIH RO1‐DK‐049750 to C.S.W and 5T32DK007518‐22 to M.M.G.