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Aldosterone induces accumulation of epithelial sodium channel α‐subunits in endosome‐like organelles of connecting tubules
Author(s) -
Cheema Muhammad Umar,
Nielsen Jakob,
Fenton Robert A.,
Praetorius Jeppe
Publication year - 2011
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.25.1_supplement.1039.19
Subject(s) - endosome , aldosterone , epithelial sodium channel , organelle , microbiology and biotechnology , chemistry , sodium , medicine , endocrinology , biophysics , biology , intracellular , organic chemistry
The epithelial sodium channel, ENaC, is a protein complex formed by α‐, β‐, and γ‐ subunits. Renal ENaC plays a crucial role in Na+ homeostasis and extracellular fluid volume. Regulation of ENaC is multifaceted and includes differential protein expression of the individual subunits and redistribution of ENaC containing vesicles to and from the apical plasma membrane. Using an antibody against the NH2‐terminus of αENaC, we previously demonstrated increased apical αENaC expression in connecting tubules and collecting duct in rats receiving 50μg aldosterone/kg body weight/24 hrs for 7 days as compared to vehicle treated controls. In this study, using an antibody against the extracellular loop of αENaC there was marked labeling of intracellular structures in connecting tubules of the aldosterone treated rats with no labeling in untreated animals. Double‐labeling immunofluorescence analysis revealed a partial colocalization of the αENaC immunoreactivity with cathepsin D (lysosomes), little with early endosomes (EEA1) and minimal with recycling endosomes (rab11). The large size of the labeled spherical structures and centrocellular position specifically in connecting tubules suggest a restriction of the immunoreactive αENaC form to the late endosomes. The results suggest that increased surface expression of αENaC is accompanied by an increased endocytosis. Supported by Lundbeck Foundation.