Role of the alternative splice variant of NCC in blood pressure control.
Publication year
2018Source
Channels, 12, 1, (2018), pp. 346-355ISSN
Publication type
Article / Letter to editor
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Organization
Physiology
Laboratory Medicine
Journal title
Channels
Volume
vol. 12
Issue
iss. 1
Page start
p. 346
Page end
p. 355
Subject
Radboudumc 11: Renal disorders RIMLS: Radboud Institute for Molecular Life SciencesAbstract
The renal thiazide-sensitive sodium-chloride cotransporter (NCC), located in the distal convoluted tubule (DCT) of the kidney, plays an important role in blood pressure regulation by fine-tuning sodium excretion. The human SLC12A3 gene, encoding NCC, gives rise to three isoforms, of which only the third isoform (NCC3) has been extensively investigated so far. However, recent studies unraveled the importance of the isoforms 1 and 2, collectively referred to as NCC splice variant (NCCSV), in several (patho)physiological conditions. In the human kidney, NCCSV localizes to the apical membrane of the DCT and could constitute a functional route for renal sodium-chloride reabsorption. Analysis of urinary extracellular vesicles (uEVs), a non-invasive method for measuring renal responses, demonstrated that NCCSV abundance changes in response to acute water loading and correlates with patients' thiazide responsiveness. Furthermore, a novel phosphorylation site at serine 811 (S811), exclusively present in NCCSV, was shown to play an instrumental role in NCCSV as well as NCC3 function. This review aims to summarize these new insights of NCCSV function in humans that broadens the understanding on NCC regulation in blood pressure control.
This item appears in the following Collection(s)
- Academic publications [238586]
- Electronic publications [122879]
- Faculty of Medical Sciences [90409]
- Open Access publications [97860]
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