Soluble vascular endothelial growth factor receptor-1 in intrauterine growth restricted fetuses and neonates
Angiogenesis, a critical process for growth and development is altered in intrauterine growth restriction (IUGR). Vascular endothelial growth factor (VEGF) and its receptors VEGFR-1, soluble (s) VEGFR-1 and VEGFR-2 represent a regulatory system, essential for both physiological and pathological angi...
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description | Angiogenesis, a critical process for growth and development is altered in intrauterine growth restriction (IUGR). Vascular endothelial growth factor (VEGF) and its receptors VEGFR-1, soluble (s) VEGFR-1 and VEGFR-2 represent a regulatory system, essential for both physiological and pathological angiogenesis.
To study the implication of sVEGFR-1–a VEGF antagonist–in IUGR.
Prospective study.
Twenty-five IUGR and 15 appropriate for gestational age (AGA) full-term fetuses and neonates with their mothers were included in the study.
sVEGFR-1 levels were determined by enzyme immunoassay in the serum of: mothers (MS), umbilical cords (UC)–representing fetal state – and neonates on day 1 (N1) and 4 (N4) of life.
MS, UC, N1 and N4 sVEGFR-1 levels in IUGR were significantly higher compared to respective AGA cases (
p
=
0.005,
p
=
0.026,
p
=
0.005 and
p
=
0.017, respectively). In IUGR and AGA groups, maternal sVEGFR-1 levels were significantly higher than fetal and neonatal levels (p in all cases <
0.001). The latter presented in both IUGR and AGA groups a significant decrease from UC to N4 (p in all cases <
0.01). MS, N1 and N4 sVEGFR-1 levels negatively correlated with the infants' customized centiles [(
r
=
−
0.489,
p
=
0.001), (
r
=
−
0.440,
p
=
0.004), (
r
=
−
0.431,
p
=
0.006), respectively].
Higher sVEGFR-1 levels in the IUGR as compared to the AGA group possibly reflect the predominance of antiangiogenic mechanisms present in IUGR. The decrease of sVEGFR-1 levels from UC to N4 may represent ex utero initiation of growth and development and therefore, prevalence of angiogenic mechanisms. |
doi_str_mv | 10.1016/j.earlhumdev.2005.09.010 |
format | Article |
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To study the implication of sVEGFR-1–a VEGF antagonist–in IUGR.
Prospective study.
Twenty-five IUGR and 15 appropriate for gestational age (AGA) full-term fetuses and neonates with their mothers were included in the study.
sVEGFR-1 levels were determined by enzyme immunoassay in the serum of: mothers (MS), umbilical cords (UC)–representing fetal state – and neonates on day 1 (N1) and 4 (N4) of life.
MS, UC, N1 and N4 sVEGFR-1 levels in IUGR were significantly higher compared to respective AGA cases (
p
=
0.005,
p
=
0.026,
p
=
0.005 and
p
=
0.017, respectively). In IUGR and AGA groups, maternal sVEGFR-1 levels were significantly higher than fetal and neonatal levels (p in all cases <
0.001). The latter presented in both IUGR and AGA groups a significant decrease from UC to N4 (p in all cases <
0.01). MS, N1 and N4 sVEGFR-1 levels negatively correlated with the infants' customized centiles [(
r
=
−
0.489,
p
=
0.001), (
r
=
−
0.440,
p
=
0.004), (
r
=
−
0.431,
p
=
0.006), respectively].
Higher sVEGFR-1 levels in the IUGR as compared to the AGA group possibly reflect the predominance of antiangiogenic mechanisms present in IUGR. The decrease of sVEGFR-1 levels from UC to N4 may represent ex utero initiation of growth and development and therefore, prevalence of angiogenic mechanisms.</description><identifier>ISSN: 0378-3782</identifier><identifier>EISSN: 1872-6232</identifier><identifier>DOI: 10.1016/j.earlhumdev.2005.09.010</identifier><identifier>PMID: 16337100</identifier><identifier>CODEN: EHDEDN</identifier><language>eng</language><publisher>Lausanne: Elsevier Ireland Ltd</publisher><subject>Adult ; Angiogenesis ; Antagonists (Biochemistry) ; Biological and medical sciences ; Care and treatment ; Embryology: invertebrates and vertebrates. Teratology ; Female ; Fetal Blood - metabolism ; Fetal Growth Retardation - blood ; Fetus ; Fetus - metabolism ; Fundamental and applied biological sciences. Psychology ; Gestational Age ; Humans ; Infant, Newborn - blood ; Intrauterine growth restriction ; Male ; Neonate ; Neovascularization ; Pregnancy - blood ; Prospective Studies ; Reference Values ; Soluble vascular endothelial growth factor receptor-1 ; Vascular Endothelial Growth Factor Receptor-1 - blood</subject><ispartof>Early human development, 2006-04, Vol.82 (4), p.235-239</ispartof><rights>2005 Elsevier Ireland Ltd</rights><rights>2006 INIST-CNRS</rights><rights>COPYRIGHT 2006 The Lancet Publishing Group, a division of Elsevier Science Ltd.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c441t-bad7f1bdacb47f26a095ddcc22d29ec7c620282273414501b92fd0d73a60e3933</citedby><cites>FETCH-LOGICAL-c441t-bad7f1bdacb47f26a095ddcc22d29ec7c620282273414501b92fd0d73a60e3933</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.earlhumdev.2005.09.010$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3536,27903,27904,45974</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17711887$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16337100$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Boutsikou, Theodora</creatorcontrib><creatorcontrib>Malamitsi-Puchner, Ariadne</creatorcontrib><creatorcontrib>Economou, Emmanuel</creatorcontrib><creatorcontrib>Boutsikou, Maria</creatorcontrib><creatorcontrib>Puchner, Karl-Philipp</creatorcontrib><creatorcontrib>Hassiakos, Dimitrios</creatorcontrib><title>Soluble vascular endothelial growth factor receptor-1 in intrauterine growth restricted fetuses and neonates</title><title>Early human development</title><addtitle>Early Hum Dev</addtitle><description>Angiogenesis, a critical process for growth and development is altered in intrauterine growth restriction (IUGR). Vascular endothelial growth factor (VEGF) and its receptors VEGFR-1, soluble (s) VEGFR-1 and VEGFR-2 represent a regulatory system, essential for both physiological and pathological angiogenesis.
To study the implication of sVEGFR-1–a VEGF antagonist–in IUGR.
Prospective study.
Twenty-five IUGR and 15 appropriate for gestational age (AGA) full-term fetuses and neonates with their mothers were included in the study.
sVEGFR-1 levels were determined by enzyme immunoassay in the serum of: mothers (MS), umbilical cords (UC)–representing fetal state – and neonates on day 1 (N1) and 4 (N4) of life.
MS, UC, N1 and N4 sVEGFR-1 levels in IUGR were significantly higher compared to respective AGA cases (
p
=
0.005,
p
=
0.026,
p
=
0.005 and
p
=
0.017, respectively). In IUGR and AGA groups, maternal sVEGFR-1 levels were significantly higher than fetal and neonatal levels (p in all cases <
0.001). The latter presented in both IUGR and AGA groups a significant decrease from UC to N4 (p in all cases <
0.01). MS, N1 and N4 sVEGFR-1 levels negatively correlated with the infants' customized centiles [(
r
=
−
0.489,
p
=
0.001), (
r
=
−
0.440,
p
=
0.004), (
r
=
−
0.431,
p
=
0.006), respectively].
Higher sVEGFR-1 levels in the IUGR as compared to the AGA group possibly reflect the predominance of antiangiogenic mechanisms present in IUGR. The decrease of sVEGFR-1 levels from UC to N4 may represent ex utero initiation of growth and development and therefore, prevalence of angiogenic mechanisms.</description><subject>Adult</subject><subject>Angiogenesis</subject><subject>Antagonists (Biochemistry)</subject><subject>Biological and medical sciences</subject><subject>Care and treatment</subject><subject>Embryology: invertebrates and vertebrates. Teratology</subject><subject>Female</subject><subject>Fetal Blood - metabolism</subject><subject>Fetal Growth Retardation - blood</subject><subject>Fetus</subject><subject>Fetus - metabolism</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gestational Age</subject><subject>Humans</subject><subject>Infant, Newborn - blood</subject><subject>Intrauterine growth restriction</subject><subject>Male</subject><subject>Neonate</subject><subject>Neovascularization</subject><subject>Pregnancy - blood</subject><subject>Prospective Studies</subject><subject>Reference Values</subject><subject>Soluble vascular endothelial growth factor receptor-1</subject><subject>Vascular Endothelial Growth Factor Receptor-1 - blood</subject><issn>0378-3782</issn><issn>1872-6232</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc2PEyEYh4nRuHX1XzBc9DYjH9OBOa6b9SPZxIN6Jgy8bGkYqMDU-N9L05oeDRAIeV74wYMQpqSnhI4f9j3oHHbrYuHYM0K2PZl6QskztKFSsG5knD1HG8KF7NpgN-hVKXvSQDmRl-iGjpwLSsgGhe8prHMAfNTFrEFnDNGmuoPgdcBPOf2uO-y0qSnjDAYObdFR7GPrNeu1QvYR_oEZSs3eVLDYQV0LFKyjxRFS1BXKa_TC6VDgzWW-RT8_Pfy4_9I9fvv89f7usTPDQGs3ayscna028yAcGzWZttYaw5hlExhhRkaYZEzwgQ5bQueJOUus4HokwCfOb9H787mHnH6tLZNafDEQgm5J1qJGISWTg2xgfwafdADlo0vtTaY1C4s3KYLzbf-ODuO2XTSeTpbnApNTKRmcOmS_6PxHUaJOatReXdWokxpFJtXUtNK3l1DrvIC9Fl5cNODdBWgqdHBZR-PLlROCUilF4z6eOWhfePSQVTEeogHrm6GqbPL_T_MXiWS0Bg</recordid><startdate>20060401</startdate><enddate>20060401</enddate><creator>Boutsikou, Theodora</creator><creator>Malamitsi-Puchner, Ariadne</creator><creator>Economou, Emmanuel</creator><creator>Boutsikou, Maria</creator><creator>Puchner, Karl-Philipp</creator><creator>Hassiakos, Dimitrios</creator><general>Elsevier Ireland Ltd</general><general>Elsevier</general><general>The Lancet Publishing Group, a division of Elsevier Science Ltd</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20060401</creationdate><title>Soluble vascular endothelial growth factor receptor-1 in intrauterine growth restricted fetuses and neonates</title><author>Boutsikou, Theodora ; Malamitsi-Puchner, Ariadne ; Economou, Emmanuel ; Boutsikou, Maria ; Puchner, Karl-Philipp ; Hassiakos, Dimitrios</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c441t-bad7f1bdacb47f26a095ddcc22d29ec7c620282273414501b92fd0d73a60e3933</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Adult</topic><topic>Angiogenesis</topic><topic>Antagonists (Biochemistry)</topic><topic>Biological and medical sciences</topic><topic>Care and treatment</topic><topic>Embryology: invertebrates and vertebrates. Teratology</topic><topic>Female</topic><topic>Fetal Blood - metabolism</topic><topic>Fetal Growth Retardation - blood</topic><topic>Fetus</topic><topic>Fetus - metabolism</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gestational Age</topic><topic>Humans</topic><topic>Infant, Newborn - blood</topic><topic>Intrauterine growth restriction</topic><topic>Male</topic><topic>Neonate</topic><topic>Neovascularization</topic><topic>Pregnancy - blood</topic><topic>Prospective Studies</topic><topic>Reference Values</topic><topic>Soluble vascular endothelial growth factor receptor-1</topic><topic>Vascular Endothelial Growth Factor Receptor-1 - blood</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Boutsikou, Theodora</creatorcontrib><creatorcontrib>Malamitsi-Puchner, Ariadne</creatorcontrib><creatorcontrib>Economou, Emmanuel</creatorcontrib><creatorcontrib>Boutsikou, Maria</creatorcontrib><creatorcontrib>Puchner, Karl-Philipp</creatorcontrib><creatorcontrib>Hassiakos, Dimitrios</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Early human development</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Boutsikou, Theodora</au><au>Malamitsi-Puchner, Ariadne</au><au>Economou, Emmanuel</au><au>Boutsikou, Maria</au><au>Puchner, Karl-Philipp</au><au>Hassiakos, Dimitrios</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Soluble vascular endothelial growth factor receptor-1 in intrauterine growth restricted fetuses and neonates</atitle><jtitle>Early human development</jtitle><addtitle>Early Hum Dev</addtitle><date>2006-04-01</date><risdate>2006</risdate><volume>82</volume><issue>4</issue><spage>235</spage><epage>239</epage><pages>235-239</pages><issn>0378-3782</issn><eissn>1872-6232</eissn><coden>EHDEDN</coden><abstract>Angiogenesis, a critical process for growth and development is altered in intrauterine growth restriction (IUGR). Vascular endothelial growth factor (VEGF) and its receptors VEGFR-1, soluble (s) VEGFR-1 and VEGFR-2 represent a regulatory system, essential for both physiological and pathological angiogenesis.
To study the implication of sVEGFR-1–a VEGF antagonist–in IUGR.
Prospective study.
Twenty-five IUGR and 15 appropriate for gestational age (AGA) full-term fetuses and neonates with their mothers were included in the study.
sVEGFR-1 levels were determined by enzyme immunoassay in the serum of: mothers (MS), umbilical cords (UC)–representing fetal state – and neonates on day 1 (N1) and 4 (N4) of life.
MS, UC, N1 and N4 sVEGFR-1 levels in IUGR were significantly higher compared to respective AGA cases (
p
=
0.005,
p
=
0.026,
p
=
0.005 and
p
=
0.017, respectively). In IUGR and AGA groups, maternal sVEGFR-1 levels were significantly higher than fetal and neonatal levels (p in all cases <
0.001). The latter presented in both IUGR and AGA groups a significant decrease from UC to N4 (p in all cases <
0.01). MS, N1 and N4 sVEGFR-1 levels negatively correlated with the infants' customized centiles [(
r
=
−
0.489,
p
=
0.001), (
r
=
−
0.440,
p
=
0.004), (
r
=
−
0.431,
p
=
0.006), respectively].
Higher sVEGFR-1 levels in the IUGR as compared to the AGA group possibly reflect the predominance of antiangiogenic mechanisms present in IUGR. The decrease of sVEGFR-1 levels from UC to N4 may represent ex utero initiation of growth and development and therefore, prevalence of angiogenic mechanisms.</abstract><cop>Lausanne</cop><cop>New York,NY</cop><cop>Amsterdam</cop><pub>Elsevier Ireland Ltd</pub><pmid>16337100</pmid><doi>10.1016/j.earlhumdev.2005.09.010</doi><tpages>5</tpages></addata></record> |
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ispartof | Early human development, 2006-04, Vol.82 (4), p.235-239 |
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language | eng |
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source | MEDLINE; Elsevier ScienceDirect Journals |
subjects | Adult Angiogenesis Antagonists (Biochemistry) Biological and medical sciences Care and treatment Embryology: invertebrates and vertebrates. Teratology Female Fetal Blood - metabolism Fetal Growth Retardation - blood Fetus Fetus - metabolism Fundamental and applied biological sciences. Psychology Gestational Age Humans Infant, Newborn - blood Intrauterine growth restriction Male Neonate Neovascularization Pregnancy - blood Prospective Studies Reference Values Soluble vascular endothelial growth factor receptor-1 Vascular Endothelial Growth Factor Receptor-1 - blood |
title | Soluble vascular endothelial growth factor receptor-1 in intrauterine growth restricted fetuses and neonates |
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