{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,28]],"date-time":"2026-08-28T13:31:15Z","timestamp":1787923875097,"version":"build-2784847793"},"reference-count":64,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,8,28]],"date-time":"2026-08-28T00:00:00Z","timestamp":1787875200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Endocrinol."],"abstract":"<jats:sec>\n                    <jats:title>Introduction<\/jats:title>\n                    <jats:p>Maternal vascular dysfunction and impaired placental angiogenesis are key features of preeclampsia (PE). Umbilical cord blood-derived endothelial colony-forming cells (CB-ECFCs) contribute to fetal endothelial repair and vascular network formation, but their phenotype in PE remains incompletely understood.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We investigated whether the matricellular protein CCN1 is associated with CB-ECFC senescence and dysfunction. CB-ECFCs were isolated from pregnancies complicated by PE (n = 8) and healthy pregnancies (n = 9). Cellular senescence was assessed by SA-\u03b2-galactosidase staining, qPCR, and Western blotting of senescence-associated markers and senescence-associated secretory phenotype factors. Control-derived CB-ECFCs were exposed to recombinant CCN1, with or without the gamma-secretase inhibitor DAPT, and senescence-associated proteins, cleaved Notch1, the redox-responsive protein HO-1, the inflammatory factor TNF-\u03b1, and the DNA damage-response marker gamma-H2AX were examined.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>PE-derived CB-ECFCs showed reduced colony yield, increased senescence-associated markers, and higher secreted and cell-associated CCN1 expression. Recombinant CCN1 increased senescence-associated markers, cleaved Notch1, HO-1, TNF-\u03b1, and \u03b3-H2AX and impaired CB-ECFC metabolic activity, migration, and tube formation. DAPT attenuated selected molecular changes and partially restored tube formation but not wound closure.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Discussion<\/jats:title>\n                    <jats:p>These findings identify increased CCN1 as a feature of PE-derived CB-ECFCs and support an association between CCN1 exposure, Notch1 signaling, oxidative stress, and CB-ECFC senescence and dysfunction. The CCN1\/Notch1 axis may represent a potential mechanism contributing to fetoplacental endothelial dysfunction in PE.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fendo.2026.1930702","type":"journal-article","created":{"date-parts":[[2026,8,28]],"date-time":"2026-08-28T12:52:47Z","timestamp":1787921567000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["CCN1-induced senescence and dysfunction of umbilical cord blood endothelial colony-forming cells in the pathogenesis of preeclampsia"],"prefix":"10.3389","volume":"17","author":[{"given":"Yuyang","family":"Ma","sequence":"first","affiliation":[{"name":"Obstetric, Gynecology and Reproductive Medicine Center, Shanghai Tenth People\u2019s Hospital, Tongji University School of Medicine","place":["Shanghai, China"]},{"name":"Center for Reproductive Medicine and Obstetric and Gynecology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, 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