{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,30]],"date-time":"2026-04-30T06:12:44Z","timestamp":1777529564886,"version":"3.51.4"},"reference-count":49,"publisher":"Oxford University Press (OUP)","issue":"3","license":[{"start":{"date-parts":[[2022,2,14]],"date-time":"2022-02-14T00:00:00Z","timestamp":1644796800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":["rep.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2022,3,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Preeclampsia is a multisystem hypertensive disorder of pregnancy that remains one of the leading causes of maternal and perinatal morbidity and mortality worldwide. The widespread maternal endothelial dysfunction that underlies preeclampsia is thought to arise from excessive placental production of various factors combined with enhanced oxidative stress. While previous studies have reported elevated activin A in women diagnosed with preeclampsia, whether activin A can cause vascular dysfunction has not yet been thoroughly investigated. Here, we demonstrated that different subtypes of activin A receptors were localised to the endothelial and smooth muscle cells of mouse and human aortae. Then, the aorta of healthy female C57Bl6J mice (n\u2009= 8) were incubated for 24 h in various concentrations of recombinant activin A to mimic early pregnancy (5 ng\/mL), late pregnancy (20 ng\/mL) and preeclampsia (50 ng\/mL). Vascular reactivity as assessed by wire myography revealed that only the preeclamptic level of activin A impaired agonist-mediated endothelium-dependent relaxation by reducing the vasodilator prostanoid contribution to relaxation. However, agonist-mediated endothelium-independent mechanisms were unaffected. Further investigations carried out on human aortic endothelial cells suggested that the impairment of aorta relaxation could also be driven by increased endothelial cell permeability, and decreased cell viability, adherence and proliferation. This is the first direct evidence to show that activin A can induce endothelial dysfunction in whole blood vessels, suggesting that at high circulating levels it may contribute to the widespread endothelial dysfunction in women with preeclampsia.<\/jats:p>","DOI":"10.1530\/rep-21-0368","type":"journal-article","created":{"date-parts":[[2022,1,17]],"date-time":"2022-01-17T14:26:26Z","timestamp":1642429586000},"page":"145-155","update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-11","source":"Crossref","is-referenced-by-count":6,"title":["Activin A causes endothelial dysfunction of mouse aorta and human aortic cells"],"prefix":"10.1093","volume":"163","author":[{"given":"Courtney","family":"Barber","sequence":"first","affiliation":[{"name":"The Ritchie Centre , Department of Obstetrics and Gynaecology, School of Clinical Sciences, Monash University, Clayton, Victoria, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yann","family":"Yap","sequence":"additional","affiliation":[{"name":"The Ritchie Centre , Department of Obstetrics and Gynaecology, School of Clinical Sciences, Monash University, Clayton, Victoria, Australia"},{"name":"The Hudson Institute of Medical Research , Clayton, Victoria, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Natalie J","family":"Hannan","sequence":"additional","affiliation":[{"name":"Translational Obstetrics Group , The Department of Obstetrics and Gynaecology, Mercy Hospital for Women, University of Melbourne & Mercy Perinatal, Mercy Hospital for Women, Heidelberg, Victoria, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Euan M","family":"Wallace","sequence":"additional","affiliation":[{"name":"The Ritchie Centre , Department of Obstetrics and Gynaecology, School of Clinical Sciences, Monash University, Clayton, Victoria, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7276-1405","authenticated-orcid":false,"given":"Sarah A","family":"Marshall","sequence":"additional","affiliation":[{"name":"The Ritchie Centre , Department of Obstetrics and Gynaecology, School of Clinical Sciences, Monash University, Clayton, Victoria, Australia"},{"name":"The Hudson Institute of Medical Research , Clayton, Victoria, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2022,2,14]]},"reference":[{"key":"2026010712084803400_bib1","doi-asserted-by":"publisher","first-page":"38","DOI":"10.3109\/08037059409101520","article-title":"Plasma and urinary endothelin 1, prostacyclin metabolites and platelet consumption in pre-eclampsia and essential hypertensive pregnancy","volume":"3","author":"Barden","year":"1994","journal-title":"Blood 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