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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Veröffentlicht in: | Early human development 2006-04, Vol.82 (4), p.235-239 |
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Zusammenfassung: | 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. |
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ISSN: | 0378-3782 1872-6232 |
DOI: | 10.1016/j.earlhumdev.2005.09.010 |