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Title: Pre-eclampsia is associated with altered expression of the renal sodium transporters NKCC2, NCC and ENaC in urinary extracellular vesicles.
Austin Authors: Hu, Chih-Chiang;Katerelos, Marina ;Choy, Suet-Wan ;Crossthwaite, Amy ;Walker, Susan P;Pell, Gabrielle;Lee, Mardiana ;Cook, Natasha ;Mount, Peter F ;Paizis, Kathy ;Power, David Anthony
Affiliation: Nephrology
Obstetrics and Gynecology, University of Melbourne, Parkville, Victoria, Australia
Department of Medicine, University of Melbourne, Parkville, Victoria, Australia
Mercy Hospital for Women, Heidelberg, Victoria, Australia
Melbourne Medical School, University of Melbourne, Parkville, Victoria, Australia
Institute for Breathing and Sleep
Issue Date: 24-Sep-2018
Date: 2018-09-24
Publication information: PLoS One 2018; 13(9): e0204514
Abstract: Pre-eclampsia is a hypertensive disorder of pregnancy characterised by hypertension and sodium retention by the kidneys. To identify changes in sodium uptake proteins in the tubules of the distal nephron, we studied their expression in urinary extracellular vesicles or exosomes (uEVs). Urine was collected from women with pre-eclampsia or during normal pregnancy, and from healthy non-pregnant controls. uEVs were isolated by centrifugation and analyzed by Western blot. Expression, proteolytic cleavage and phosphorylation was determined by densitometric analysis normalized to the exosome marker CD9. Results showed a significant increase in phosphorylation of the activating S130 site in NKCC2, the drug target for frusemide, in women with pre-eclampsia compared with normal pregnant women. Phosphorylation of the activating sites T101/105 in NKCC2 was similar but the activating T60 site in NCC, the drug target for thiazide diuretics, showed significantly less phosphorylation in pre-eclampsia compared with normal pregnancy. Expression of the larger forms of the α subunit of ENaC, the drug target for amiloride, was significantly greater in pre-eclampsia, with more fragmentation of theγ subunit. The differences observed are predicted to increase the activity of NKCC2 and ENaC while reducing that of NCC. This will increase sodium reabsorption, and so contribute to hypertension in pre-eclampsia.
DOI: 10.1371/journal.pone.0204514
ORCID: 0000-0001-7637-3661
Journal: PLoS One
PubMed URL: 30248150
Type: Journal Article
Appears in Collections:Journal articles

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