Mistry, Hiten D; Klossner, Rahel; Scaife, Paula J; Eisele, Nicole; Kurlak, Lesia O; Kallol, Sampada; Albrecht, Christiane; Gennari-Moser, Carine; Briggs, Louise V; Broughton Pipkin, Fiona; Mohaupt, Markus G (2024). Alterations of Placental Sodium in Preeclampsia: Trophoblast Responses. Hypertension, 81(9), pp. 1924-1934. American Heart Association 10.1161/HYPERTENSIONAHA.124.23001
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mistry-et-al-2024-alterations-of-placental-sodium-in-preeclampsia-trophoblast-responses.pdf - Published Version Available under License Creative Commons: Attribution (CC-BY). Download (785kB) | Preview |
BACKGROUND
Evidence suggests that increasing salt intake in pregnancy lowers blood pressure, protecting against preeclampsia. We hypothesized that sodium (Na+) evokes beneficial placental signals that are disrupted in preeclampsia.
METHODS
Blood and urine were collected from nonpregnant women of reproductive age (n=26) and pregnant women with (n=50) and without (n=55) preeclampsia, along with placental biopsies. Human trophoblast cell lines and primary human trophoblasts were cultured with varying Na+ concentrations.
RESULTS
Women with preeclampsia had reduced placental and urinary Na+ concentrations, yet increased urinary angiotensinogen and reduced active renin, aldosterone concentrations, and osmotic response signal TonEBP (tonicity-responsive enhancer binding protein) expression. In trophoblast cell cultures, TonEBP was consistently increased upon augmented Na+ exposure. Mechanistically, inhibiting Na+/K+-ATPase or adding mannitol evoked the TonEBP response, whereas inhibition of cytoskeletal signaling abolished it.
CONCLUSIONS
Enhanced Na+ availability induced osmotic gradient-dependent cytoskeletal signals in trophoblasts, resulting in proangiogenic responses. As placental salt availability is compromised in preeclampsia, adverse systemic responses are thus conceivable.
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