Aldosterone modulates the association between NCC and ENAC

Wynne, Brandi M.; Mistry, Abinash C.; Al-Khalili, Otor; Mallick, Rickta; Theilig, Franziska; Eaton, Douglas C.; Hoover, Robert S.

doi:10.1038/s41598-017-03510-5

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Journal article

Aldosterone modulates the association between NCC and ENAC

Wynne, Brandi M. Division of Nephrology, Department of Medicine, Emory University, Atlanta, USA - Center for Cell and Molecular Signaling, Emory University, Atlanta, USA
Mistry, Abinash C. Division of Nephrology, Department of Medicine, Emory University, Atlanta, USA
Al-Khalili, Otor Department of Physiology, Emory University, Atlanta, USA
Mallick, Rickta Division of Nephrology, Department of Medicine, Emory University, Atlanta, USA
Theilig, Franziska Department of Medicine, University of Fribourg, Fribourg, Switzerland
Eaton, Douglas C. Department of Physiology, Emory University, Atlanta, USA - Center for Cell and Molecular Signaling, Emory University, Atlanta, USA
Hoover, Robert S. Division of Nephrology, Department of Medicine, Emory University, Atlanta, USA - Department of Physiology, Emory University, Atlanta, USA - Research Service, Atlanta Veteran’s Administration Medical Center, Decatur, USA

23.06.2017

Published in:

Scientific Reports. - 2017, vol. 7, no. 1, p. 4149

English Distal sodium transport is a final step in the regulation of blood pressure. As such, understanding how the two main sodium transport proteins, the thiazide-sensitive sodium chloride cotransporter (NCC) and the epithelial sodium channel (ENaC), are regulated is paramount. Both are expressed in the late distal nephron; however, no evidence has suggested that these two sodium transport proteins interact. Recently, we established that these two sodium transport proteins functionally interact in the second part of the distal nephron (DCT2). Given their co-localization within the DCT2, we hypothesized that NCC and ENaC interactions might be modulated by aldosterone (Aldo). Aldo treatment increased NCC and αENaC colocalization (electron microscopy) and interaction (coimmunoprecipitation). Finally, with co-expression of the Aldo-induced protein serum- and glucocorticoid-inducible kinase 1 (SGK1), NCC and αENaC interactions were increased. These data demonstrate that Aldo promotes increased interaction of NCC and ENaC, within the DCT2 revealing a novel method of regulation for distal sodium reabsorption.

Faculty

Faculté des sciences et de médecine

Department

Département de Médecine

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