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2017 ; 7
(1
): 4149
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Aldosterone Modulates the Association between NCC and ENaC
#MMPMID28646163
Wynne BM
; Mistry AC
; Al-Khalili O
; Mallick R
; Theilig F
; Eaton DC
; Hoover RS
Sci Rep
2017[Jun]; 7
(1
): 4149
PMID28646163
show ga
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 ?ENaC colocalization (electron microscopy) and interaction
(coimmunoprecipitation). Finally, with co-expression of the Aldo-induced protein
serum- and glucocorticoid-inducible kinase 1 (SGK1), NCC and ?ENaC 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.
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