Ouabain protects against adverse developmental programming of the kidney

Juan Li, Georgiy R. Khodus, Markus Kruusmägi, Padideh Kamali-Zare, Xiao-Li Liu, Ann-Christine Eklöf, Sergey Zelenin, Hjalmar Brismar and Anita Aperia ()
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Juan Li: Karolinska Institutet
Georgiy R. Khodus: Karolinska Institutet
Markus Kruusmägi: Karolinska Institutet
Padideh Kamali-Zare: Royal Institute of Technology
Xiao-Li Liu: Karolinska Institutet
Ann-Christine Eklöf: Karolinska Institutet
Sergey Zelenin: Karolinska Institutet
Hjalmar Brismar: Karolinska Institutet
Anita Aperia: Karolinska Institutet

Nature Communications, 2010, vol. 1, issue 1, 1-7

Abstract: Abstract The kidney is extraordinarily sensitive to adverse fetal programming. Malnutrition, the most common form of developmental challenge, retards the formation of functional units, the nephrons. The resulting low nephron endowment increases susceptibility to renal injury and disease. Using explanted rat embryonic kidneys, we found that ouabain, the Na,K-ATPase ligand, triggers a calcium–nuclear factor-κB signal, which protects kidney development from adverse effects of malnutrition. To mimic malnutrition, kidneys were serum deprived for 24 h. This resulted in severe retardation of nephron formation and a robust increase in apoptosis. In ouabain-exposed kidneys, no adverse effects of serum deprivation were observed. Proof of principle that ouabain rescues development of embryonic kidneys exposed to malnutrition was obtained from studies on pregnant rats given a low-protein diet and treated with ouabain or vehicle throughout pregnancy. Thus, we have identified a survival signal and a feasible therapeutic tool to prevent adverse programming of kidney development.

Date: 2010
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DOI: 10.1038/ncomms1043

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