Preliminary evidence that blocking the uptake of placenta-derived preeclamptic extracellular vesicles protects the vascular endothelium and prevents vasoconstriction.


Journal

Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288

Informations de publication

Date de publication:
27 10 2023
Historique:
received: 18 07 2023
accepted: 24 10 2023
medline: 30 10 2023
pubmed: 28 10 2023
entrez: 27 10 2023
Statut: epublish

Résumé

Preeclampsia (PE) is a pregnancy syndrome characterized by hypertension and organ damage manifesting after 20 gestational weeks. The etiology is of multifactorial origin, where placental stress causes increased levels of placenta-derived extracellular vesicles (STBEVs) in the maternal circulation, shown to cause inflammation, endothelial activation, vasoconstriction, and anti-angiogenic activity. General endothelial dysfunction is believed to be initiated by endothelial insult during pregnancy that alters vascular function resulting in increased arterial stiffness, cardiac dysfunction, and increased risk of cardiovascular disease later in life. We compared the effect of normal and PE derived STBEVs in vitro on vascular contractility of human subcutaneous arteries using wire myography. Cellular structures of exposed vessels were investigated by transmission electron microscopy. We explored strategies to pharmacologically block the effects of the STBEVs on human vessels. The PE STBEVs caused significantly stronger angiotensin II-mediated contractions and extended structural damage to human subcutaneous arteries compared to normal STBEVs. These negative effects could be reduced by blocking vesicle uptake by endothelial cells, using chlorpromazine or specific antibodies towards the LOX-1 receptor. The therapeutic potential of blocking vesicle uptake should be further explored, to reduce the permanent damage caused on the vasculature during PE pregnancy to prevent future cardiovascular risk.

Identifiants

pubmed: 37891193
doi: 10.1038/s41598-023-45830-9
pii: 10.1038/s41598-023-45830-9
pmc: PMC10611745
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

18425

Informations de copyright

© 2023. The Author(s).

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Auteurs

Lena Erlandsson (L)

Division of Obstetrics and Gynecology, Department of Clinical Sciences Lund, Lund University, BMC C14, Klinikgatan 28, 221 85, Lund, Sweden. lena.erlandsson@med.lu.se.

Lena Ohlsson (L)

Experimental Vascular Research, Department of Clinical Sciences Lund, Lund University, Lund, Sweden.

Zahra Masoumi (Z)

Division of Obstetrics and Gynecology, Department of Clinical Sciences Lund, Lund University, BMC C14, Klinikgatan 28, 221 85, Lund, Sweden.

Mimmi Rehnström (M)

Division of Obstetrics and Gynecology, Department of Clinical Sciences Lund, Lund University, BMC C14, Klinikgatan 28, 221 85, Lund, Sweden.

Tina Cronqvist (T)

Division of Obstetrics and Gynecology, Department of Clinical Sciences Lund, Lund University, BMC C14, Klinikgatan 28, 221 85, Lund, Sweden.

Lars Edvinsson (L)

Experimental Vascular Research, Department of Clinical Sciences Lund, Lund University, Lund, Sweden.
Skåne University Hospital, Lund, Sweden.

Stefan R Hansson (SR)

Division of Obstetrics and Gynecology, Department of Clinical Sciences Lund, Lund University, BMC C14, Klinikgatan 28, 221 85, Lund, Sweden.
Skåne University Hospital, Lund, Sweden.

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