1. Decreased placental expression of hPGH, IGF-I and IGFBP-1 in pregnancies complicated by fetal growth restriction.
- Author
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Koutsaki M, Sifakis S, Zaravinos A, Koutroulakis D, Koukoura O, and Spandidos DA
- Subjects
- Adolescent, Adult, Case-Control Studies, Down-Regulation genetics, Female, Fetal Growth Retardation metabolism, Fetal Growth Retardation pathology, Gene Expression Regulation, Human Growth Hormone metabolism, Humans, Insulin-Like Growth Factor Binding Protein 1 metabolism, Insulin-Like Growth Factor I metabolism, Placenta pathology, Placental Hormones genetics, Placental Hormones metabolism, Pregnancy, Young Adult, Fetal Growth Retardation genetics, Human Growth Hormone genetics, Insulin-Like Growth Factor Binding Protein 1 genetics, Insulin-Like Growth Factor I genetics, Placenta metabolism
- Abstract
Objective: The human Placental Growth Hormone (hPGH) and the Insulin-like Growth Factor (IGF) system are implicated in fetal development. This study aimed to evaluate the expression of hPGH, IGF-I, IGFBP-1 and IGFBP-3 genes in placentas from pregnancies complicated by fetal growth restriction (FGR)., Design: The study group was comprised of term placentas from 47 FGR-complicated pregnancies of no recognizable cause. Thirty-seven placentas from normal pregnancies with appropriate for gestational age birth weight were used as controls. The expression status of the genes was evaluated by quantitative real-time PCR., Results: hPGH, IGF-I and IGFBP-1 exhibited significantly lower expression compared to the controls (p=0.003, p=0.049 and p=0.001, respectively). Numerically, lower IGFBP-3 expression was also demonstrated in the FGR-affected group, without however reaching statistical significance (p=0.129). Significant co-expression patterns were detected among the study genes in both the FGR and normal pregnancies., Conclusion: Decreased placental expression levels of hPGH, IGF-I and IGFBP-1 were demonstrated in pregnancies with FGR. Whether these alterations are a causative factor of FGR or accompany other pathogenetic mechanisms requires further investigation., (Copyright © 2010 Growth Hormone Research Society. Published by Elsevier Ltd. All rights reserved.)
- Published
- 2011
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