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Activation of Na,KATPase signaling protects against glomerulo‐tubular disconnection
Author(s) -
Burlaka Ievgeniia,
Holtback Ulla,
Liu Xiao Li,
Eklof Ann-Christine,
Fogo Agnes,
Aperia Anita
Publication year - 2012
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.26.1_supplement.lb463
Subject(s) - disconnection , ouabain , apoptosis , chemistry , proteinuria , podocyte , medicine , nephritis , endocrinology , kidney , microbiology and biotechnology , biology , biochemistry , organic chemistry , political science , law , sodium
Glomerulo‐tubular disconnection and formation of atubular glomeruli is a common feature in glomerular and tubular disorders and is believed to contribute to progression of renal disease. Apoptosis of proximal tubular cells caused by proteinuria is considered a main cause of the disconnection. Our group has identified a novel signaling system in the kidney that is activated by ouabain and involves Na,K‐ATPase and the inositol 1,4,5‐triphosphate receptor. Downstream effects include activation of antiapoptotic factor Bcl‐xL and protection from apoptosis. Here we have examined whether chronic ouabain treatment prevents glomerulo‐tubular disconnections in rats with Passive Heymann Nephritis (PHN), followed for 4 months. Rats received ouabain (15 μg/kg/day) or vehicle via mini pumps. The number of apoptotic cells at the glomerulo‐tubular disconnection, number of atubular glomeruli and serum creatinine were significantly lower in PHN/ouabain than in PHN/vehicle rats. Conclusion Proteinuria‐induced apoptosis and glomerulo‐tubular disconnection can be alleviated by the antiapoptotic signaling pathway triggered by ouabain.