{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,6]],"date-time":"2026-11-06T20:22:46Z","timestamp":1793996566521,"version":"4.8.0"},"reference-count":40,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"6","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Hypertension"],"published-print":{"date-parts":[[2013,12]]},"abstract":"<jats:p>\n                    Failure to transform uteroplacental spiral arteries is thought to underpin disorders of pregnancy, including preeclampsia and fetal growth restriction (FGR). In this study, spiral artery remodeling and extravillous-cytotrophoblast were examined in placental bed biopsies from normal pregnancy (n=25), preeclampsia (n=22), and severe FGR (n=10) and then compared with clinical parameters. Biopsies were immunostained to determine vessel wall integrity, extravillous-cytotrophoblast location\/density, periarterial fibrinoid, and endothelium. Muscle disruption was reduced in myometrial spiral arteries in preeclampsia (\n                    <jats:italic>P<\/jats:italic>\n                    =0.0001) and FGR (\n                    <jats:italic>P<\/jats:italic>\n                    =0.0001) compared with controls. Myometrial vessels from cases with birth weight &lt;5th percentile (\n                    <jats:italic>P<\/jats:italic>\n                    &lt;0.001), abnormal uterine Doppler (\n                    <jats:italic>P<\/jats:italic>\n                    &lt;0.01), abnormal umbilical artery Doppler (\n                    <jats:italic>P<\/jats:italic>\n                    &lt;0.001), and preterm delivery (\n                    <jats:italic>P<\/jats:italic>\n                    &lt;0.001) had less muscle destruction compared with &gt;5th percentile. Fewer extravillous-cytotrophoblast surrounded both decidual and myometrial vessels in the normal group and preeclampsia group compared with the FGR group (\n                    <jats:italic>P<\/jats:italic>\n                    =0.001). For myometrial vessels, the normal group contained more intramural extravillous-cytotrophoblast than in preeclampsia (\n                    <jats:italic>P<\/jats:italic>\n                    =0.015). Decidual vessels in the FGR group had less fibrinoid deposition compared with controls (\n                    <jats:italic>P<\/jats:italic>\n                    =0.013). For myometrial vessels, less fibrinoid was deposited in both the preeclampsia group (\n                    <jats:italic>P<\/jats:italic>\n                    =0.0001) and the FGR group (\n                    <jats:italic>P<\/jats:italic>\n                    =0.01) when compared with controls, and less fibrinoid was deposited in the preeclampsia group when compared with FGR group (\n                    <jats:italic>P<\/jats:italic>\n                    &lt;0.001). Myometrial vessels obtained from birth weights &lt;5th percentile had less periarterial fibrinoid than those with &gt;5th percentile (\n                    <jats:italic>P<\/jats:italic>\n                    &lt;0.02). A major defect in myometrial spiral artery remodeling occurs in preeclampsia and FGR that is linked to clinical parameters. Interstitial extravillous-cytotrophoblast is not reduced in preeclampsia but is increased in FGR.\n                  <\/jats:p>","DOI":"10.1161\/hypertensionaha.113.01892","type":"journal-article","created":{"date-parts":[[2013,9,24]],"date-time":"2013-09-24T01:28:12Z","timestamp":1379986092000},"page":"1046-1054","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":483,"title":["Spiral Artery Remodeling and Trophoblast Invasion in Preeclampsia and Fetal Growth Restriction"],"prefix":"10.1161","volume":"62","author":[{"given":"Fiona","family":"Lyall","sequence":"first","affiliation":[{"name":"From the Institute of Medical Genetics, College of Medicine, Veterinary and Life Sciences, University of Glasgow School of Medicine, Glasgow, United Kingdom (F.L.); and Reproductive and Vascular Biology Group, Institute of Cellular Medicine, The Medical School, Newcastle University, Newcastle upon Tyne, United Kingdom (J.N.B., S.R.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stephen C.","family":"Robson","sequence":"additional","affiliation":[{"name":"From the Institute of Medical Genetics, College of Medicine, Veterinary and Life Sciences, University of Glasgow School of Medicine, Glasgow, United Kingdom (F.L.); and Reproductive and Vascular Biology Group, Institute of Cellular Medicine, The Medical School, Newcastle University, Newcastle upon Tyne, United Kingdom (J.N.B., S.R.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Judith N.","family":"Bulmer","sequence":"additional","affiliation":[{"name":"From the Institute of Medical Genetics, College of Medicine, Veterinary and Life Sciences, University of Glasgow School of Medicine, Glasgow, United Kingdom (F.L.); and Reproductive and Vascular Biology Group, Institute of Cellular Medicine, The Medical School, Newcastle University, Newcastle upon Tyne, United Kingdom (J.N.B., S.R.)."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_4_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.placenta.2005.12.006"},{"key":"e_1_3_4_3_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.1111726"},{"key":"e_1_3_4_4_2","doi-asserted-by":"publisher","DOI":"10.1093\/bmb\/ldg005"},{"key":"e_1_3_4_5_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(05)17987-2"},{"key":"e_1_3_4_6_2","doi-asserted-by":"publisher","DOI":"10.1161\/hypertensionaha.110.157743"},{"key":"e_1_3_4_7_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1471-0528.1986.tb07830.x"},{"key":"e_1_3_4_8_2","doi-asserted-by":"publisher","DOI":"10.1159\/000406847"},{"key":"e_1_3_4_9_2","first-page":"3","volume-title":"Pre-eclampsia; Etiology and Clinical Practice","author":"Pijnenborg R","year":"2007","unstructured":"Pijnenborg R, Vercruysse L, Hanssens M, Van Assche F A. 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