The role of insulin-like growth factor binding protein-1 phosphoisoforms in pregnancies with impaired placental function identified by Doppler ultrasound

Citation
D. Fowler et al., The role of insulin-like growth factor binding protein-1 phosphoisoforms in pregnancies with impaired placental function identified by Doppler ultrasound, HUM REPR, 14(11), 1999, pp. 2881-2885
Citations number
28
Categorie Soggetti
Reproductive Medicine","da verificare
Journal title
HUMAN REPRODUCTION
ISSN journal
02681161 → ACNP
Volume
14
Issue
11
Year of publication
1999
Pages
2881 - 2885
Database
ISI
SICI code
0268-1161(199911)14:11<2881:TROIGF>2.0.ZU;2-7
Abstract
This study was performed to investigate the hypothesis that insulin-like gr owth factor binding protein-1 (IGFBP-1) is involved in the pathogenesis of trophoblast invasion and impaired placentation in human pregnancy. The role of total and non-phosphorylated IGFBP-1. in women with fetal growth restri ction and in high risk pregnancies identified by uterine artery Doppler ult rasound screening was examined. This was a prospective study of women booke d for antenatal care having second trimester anomaly scans and Doppler scre ening between 22-26 weeks gestation. Women were divided into three groups a nd compared: normal uterine artery Doppler and normal fetal growth (control group, n = 10); abnormal Doppler and normal fetal growth [bilateral uterin e artery notches (BN; n = 16); abnormal Doppler and intrauterine growth res triction (IUGR; n = 8)]. Maternal serum was collected, stored and assayed s imultaneously for total and non-phosphorylated IGFBP-1. There was elevated total and non-phosphorylated IGFBP-1 (mean 44.99 +/- 12.19 and 29.61 +/- 10 .38 mu g/l respectively) in the IUGR group compared with controls (mean 17. 96 +/- 3.24 and 12.18 +/- 1.55 mu g/l, P < 0.05). This finding suggests tha t the various IGFBP-1 isoforms, the degree of phosphorylation and the ratio s of these different forms locally may be important during trophoblast inva sion and may be implicated in clinical manifestations of impaired placentat ion later in the second trimester.