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Article: Expression of vascular endothelial growth factor in third-trimester placentas is not increased in growth-restricted fetuses

TitleExpression of vascular endothelial growth factor in third-trimester placentas is not increased in growth-restricted fetuses
Authors
Issue Date2001
PublisherSage Publications, Inc. The Journal's web site is located at http://rsx.sagepub.com
Citation
Journal Of The Society For Gynecologic Investigation, 2001, v. 8 n. 2, p. 77-82 How to Cite?
AbstractObjective: Vascular endothelial growth factor (VEGF) is considered the growth factor that stimulates vasculogenesis and angiogenesis. Recent studies have demonstrated its role in regulating placental growth and invasion. Its expression can be upregulated by hypoxia. Intrauterine growth restriction (IUGR) is thought to be associated with inadequate placental perfusion, which might result from a failure in the development of the villous vascular network. Our present study was undertaken to examine the relationship between VEGF expression and IUGR in pregnancies with preserved umbilical artery end-diastolic flow. Methods: VEGF Expression was determined by immunohistochemical analysis of placentas from 17 pregnancies with normal infant birth weight and 17 pregnancies complicated by IUGR. Results: We found no significant differences in the expression of VEGF in villous syncytiotrophoblasts and intermediate trophoblasts in maternal decidua between IUGR and normal pregnancies. However, in both groups there was a strong correlation in the expression of VEGF with villous syncytiotrophoblasts and intermediate trophoblasts. In normal and IUGR pregnancies the infants' Apgar scores at birth were significantly correlated with VEGF staining in both syncytiotrophoblasts and intermediate trophoblasts (P < .05). A strong correlation also was found between cord hematocrit and VEGF staining in villous syncytiotrophoblasts (P < .05), but VEGF staining in intermediate trophoblasts was not correlated with cord hemoglobin or hematocrit. Conclusions: Our results suggest that VEGF acts in an autocrine and paracrine fashion in both normal and IUGR placentas, and its expression can have an effect on the well being of the infant at birth. Copyright © 2001 Society for Gynecologic Investigation.
Persistent Identifierhttp://hdl.handle.net/10722/88339
ISSN
2008 Impact Factor: 2.333
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTse, JYMen_HK
dc.contributor.authorLao, TTen_HK
dc.contributor.authorChan, CCWen_HK
dc.contributor.authorChiu, PMen_HK
dc.contributor.authorCheung, ANYen_HK
dc.date.accessioned2010-09-06T09:42:05Z-
dc.date.available2010-09-06T09:42:05Z-
dc.date.issued2001en_HK
dc.identifier.citationJournal Of The Society For Gynecologic Investigation, 2001, v. 8 n. 2, p. 77-82en_HK
dc.identifier.issn1071-5576en_HK
dc.identifier.urihttp://hdl.handle.net/10722/88339-
dc.description.abstractObjective: Vascular endothelial growth factor (VEGF) is considered the growth factor that stimulates vasculogenesis and angiogenesis. Recent studies have demonstrated its role in regulating placental growth and invasion. Its expression can be upregulated by hypoxia. Intrauterine growth restriction (IUGR) is thought to be associated with inadequate placental perfusion, which might result from a failure in the development of the villous vascular network. Our present study was undertaken to examine the relationship between VEGF expression and IUGR in pregnancies with preserved umbilical artery end-diastolic flow. Methods: VEGF Expression was determined by immunohistochemical analysis of placentas from 17 pregnancies with normal infant birth weight and 17 pregnancies complicated by IUGR. Results: We found no significant differences in the expression of VEGF in villous syncytiotrophoblasts and intermediate trophoblasts in maternal decidua between IUGR and normal pregnancies. However, in both groups there was a strong correlation in the expression of VEGF with villous syncytiotrophoblasts and intermediate trophoblasts. In normal and IUGR pregnancies the infants' Apgar scores at birth were significantly correlated with VEGF staining in both syncytiotrophoblasts and intermediate trophoblasts (P < .05). A strong correlation also was found between cord hematocrit and VEGF staining in villous syncytiotrophoblasts (P < .05), but VEGF staining in intermediate trophoblasts was not correlated with cord hemoglobin or hematocrit. Conclusions: Our results suggest that VEGF acts in an autocrine and paracrine fashion in both normal and IUGR placentas, and its expression can have an effect on the well being of the infant at birth. Copyright © 2001 Society for Gynecologic Investigation.en_HK
dc.languageengen_HK
dc.publisherSage Publications, Inc. The Journal's web site is located at http://rsx.sagepub.comen_HK
dc.relation.ispartofJournal of the Society for Gynecologic Investigationen_HK
dc.rightsJournal of the Society for Gynecologic Investigation. Copyright © Sage Publications, Inc.en_HK
dc.subject.meshBirth Weighten_HK
dc.subject.meshEndothelial Growth Factors - analysisen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshFetal Growth Retardation - metabolismen_HK
dc.subject.meshGestational Ageen_HK
dc.subject.meshHumansen_HK
dc.subject.meshImmunohistochemistryen_HK
dc.subject.meshLymphokines - analysisen_HK
dc.subject.meshOrgan Sizeen_HK
dc.subject.meshPlacenta - anatomy & histology - chemistryen_HK
dc.subject.meshPregnancyen_HK
dc.subject.meshTrophoblasts - chemistryen_HK
dc.subject.meshVascular Endothelial Growth Factor Aen_HK
dc.subject.meshVascular Endothelial Growth Factorsen_HK
dc.titleExpression of vascular endothelial growth factor in third-trimester placentas is not increased in growth-restricted fetusesen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1071-5576&volume=8&issue=2&spage=77&epage=82&date=2001&atitle=Expression+of+vascular+endothelial+growth+factor+in+third-trimester+placentas+is+not+increased+in+growth-restricted+fetusesen_HK
dc.identifier.emailCheung, ANY:anycheun@hkucc.hku.hken_HK
dc.identifier.authorityCheung, ANY=rp00542en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/S1071-5576(01)00096-Xen_HK
dc.identifier.pmid11336877-
dc.identifier.scopuseid_2-s2.0-0035032042en_HK
dc.identifier.hkuros57196en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0035032042&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume8en_HK
dc.identifier.issue2en_HK
dc.identifier.spage77en_HK
dc.identifier.epage82en_HK
dc.identifier.isiWOS:000168357400003-
dc.publisher.placeUnited Statesen_HK

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