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Microarray analysis of placental tissue in intrauterine growth restriction.
Clin Endocrinol (Oxf) 2010; 72(2):241-7CE

Abstract

OBJECTIVE

Besides foetal or maternal disorders, placental dysfunction is a major cause of intrauterine growth restriction (IUGR). Although numerous macro- and histopathological changes have been described, little is known about the precise aetiology and the contribution of foetal/placental genes in this disorder.

DESIGN

Placental tissues of 20 IUGR and control neonates were analysed by microarray technique. Four of the regulated genes with possible relevance in the pathogenesis of IUGR and its consequences were further studied in placentas of 27 IUGR and 35 control newborns.

RESULTS

Elevated gene expression of leptin, corticotrophin-releasing hormone (CRH), and IGF-binding protein-1 (IGFBP-1) in IUGR placentas could be confirmed in the larger group by real-time PCR, whereas prolactin showed no significant difference. Accordingly, protein expression of leptin and IGFBP-1 depicted by Western blot was elevated in IUGR, prolactin was not different. Birthweight standard deviation score (SDS) correlated negatively to leptin, IGFBP-1, and CRH, whereas placental weight correlated only to IGFBP-1. Leptin correlated negatively to gestational age of IUGR patients and positively to placental score, a marker of severity of impaired foeto-placental circulation.

CONCLUSIONS

As confirmed in a large group of IUGR and control samples, the up-regulated factors leptin, IGFBP-1, and CRH may serve as candidate genes for the prediction of subsequent metabolic consequences in IUGR newborns. These three factors may not only influence growth of the foetus, but might also interact with programming of its metabolic functions, which has to be determined in an ongoing study.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

19548955

Citation

Struwe, E, et al. "Microarray Analysis of Placental Tissue in Intrauterine Growth Restriction." Clinical Endocrinology, vol. 72, no. 2, 2010, pp. 241-7.
Struwe E, Berzl G, Schild R, et al. Microarray analysis of placental tissue in intrauterine growth restriction. Clin Endocrinol (Oxf). 2010;72(2):241-7.
Struwe, E., Berzl, G., Schild, R., Blessing, H., Drexel, L., Hauck, B., ... Dötsch, J. (2010). Microarray analysis of placental tissue in intrauterine growth restriction. Clinical Endocrinology, 72(2), pp. 241-7. doi:10.1111/j.1365-2265.2009.03659.x.
Struwe E, et al. Microarray Analysis of Placental Tissue in Intrauterine Growth Restriction. Clin Endocrinol (Oxf). 2010;72(2):241-7. PubMed PMID: 19548955.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Microarray analysis of placental tissue in intrauterine growth restriction. AU - Struwe,E, AU - Berzl,G, AU - Schild,R, AU - Blessing,H, AU - Drexel,L, AU - Hauck,B, AU - Tzschoppe,A, AU - Weidinger,M, AU - Sachs,M, AU - Scheler,C, AU - Schleussner,E, AU - Dötsch,J, Y1 - 2009/06/22/ PY - 2009/6/25/entrez PY - 2009/6/25/pubmed PY - 2010/8/26/medline SP - 241 EP - 7 JF - Clinical endocrinology JO - Clin. Endocrinol. (Oxf) VL - 72 IS - 2 N2 - OBJECTIVE: Besides foetal or maternal disorders, placental dysfunction is a major cause of intrauterine growth restriction (IUGR). Although numerous macro- and histopathological changes have been described, little is known about the precise aetiology and the contribution of foetal/placental genes in this disorder. DESIGN: Placental tissues of 20 IUGR and control neonates were analysed by microarray technique. Four of the regulated genes with possible relevance in the pathogenesis of IUGR and its consequences were further studied in placentas of 27 IUGR and 35 control newborns. RESULTS: Elevated gene expression of leptin, corticotrophin-releasing hormone (CRH), and IGF-binding protein-1 (IGFBP-1) in IUGR placentas could be confirmed in the larger group by real-time PCR, whereas prolactin showed no significant difference. Accordingly, protein expression of leptin and IGFBP-1 depicted by Western blot was elevated in IUGR, prolactin was not different. Birthweight standard deviation score (SDS) correlated negatively to leptin, IGFBP-1, and CRH, whereas placental weight correlated only to IGFBP-1. Leptin correlated negatively to gestational age of IUGR patients and positively to placental score, a marker of severity of impaired foeto-placental circulation. CONCLUSIONS: As confirmed in a large group of IUGR and control samples, the up-regulated factors leptin, IGFBP-1, and CRH may serve as candidate genes for the prediction of subsequent metabolic consequences in IUGR newborns. These three factors may not only influence growth of the foetus, but might also interact with programming of its metabolic functions, which has to be determined in an ongoing study. SN - 1365-2265 UR - https://www.unboundmedicine.com/medline/citation/19548955/Microarray_analysis_of_placental_tissue_in_intrauterine_growth_restriction_ L2 - https://doi.org/10.1111/j.1365-2265.2009.03659.x DB - PRIME DP - Unbound Medicine ER -