Fetus-Placenta-Newborn
Preterm fetal growth restriction is associated with increased parathyroid hormone–related protein expression in the fetal membranes,☆☆

https://doi.org/10.1067/mob.2000.106593Get rights and content

Abstract

Objective: Parathyroid hormone–related protein has roles in normal fetal growth, placental calcium transport, and vascular tone regulation; these factors are compromised in growth-restricted fetuses. Our objective was to determine whether intrauterine parathyroid hormone–related protein expression was increased in association with fetal growth restriction. Study Design: The expression of parathyroid hormone–related protein was examined in intrauterine tissues from women with idiopathic fetal growth restriction with preterm (n = 8-10) and term (n = 8-10) gestations and from gestation-matched control subjects. The abundance and immunoreactive content of parathyroid hormone–related protein messenger ribonucleic acid were determined by Northern blot and radioimmunoassay, respectively, in the placenta, amnion, and chorion-decidua. Results: The expression of parathyroid hormone–related protein messenger ribonucleic acid was increased in the amnion (placental and reflected) in association with preterm fetal growth restriction (P <.05). Both parathyroid hormone–related protein messenger ribonucleic acid and protein expression were increased in chorion-decidua in association with preterm fetal growth restriction (P <.05). In term gestations both parathyroid hormone–related protein messenger ribonucleic acid and protein expression were greater in amnion over placenta than in reflected amnion (P <.05); these in turn were greater than those in chorion-decidua (P <.05). No significant changes were detected in parathyroid hormone–related protein messenger ribonucleic acid or in protein expression in association with term fetal growth restriction. Conclusion: Either parathyroid hormone–related protein messenger ribonucleic acid or protein expression, or both, was increased in the fetal membranes in association with fetal growth restriction in preterm but not term gestations, suggesting that parathyroid hormone–related protein may be involved in the pathogenesis of preterm fetal growth restriction. (Am J Obstet Gynecol 2000;183:700-5.)

Section snippets

Patients and tissue collection

This project was approved by the Royal Women’s Hospital research and ethics committees, and written, informed consent was obtained from participating patients. Placentas and fetal membranes were collected at delivery from either preterm (26-36 weeks) or term (37-42 weeks) gestation from women with growth-restricted fetuses and from control subjects with normal pregnancies. Preterm control deliveries resulted from spontaneous preterm labor (no infection) and subsequent delivery of neonates with

Results

For some patients, because of limited available tissue (particularly amnion), it was not possible to carry out both Northern blot and radioimmunoassay analyses; thus clinical information is presented separately for these 2 data sets (Table I).

. Relevant clinical information for tissues collected from pregnancies with fetal growth restriction and from normal control pregnancies

Clinical groupNo.Gestation (wk)Birth weight (kg)Placental weight (g)Fetal/placental weight ratio
Northern blot data
 Preterm

Comment

We hypothesized that the expression of PTHrP in intrauterine tissues would be increased in association with fetal growth restriction. The data obtained in this study demonstrate that the expression of either PTHrP or its messenger RNA, or both, was elevated in the fetal membranes in association with preterm fetal growth restriction. There were no changes in PTHrP expression observed in association with term fetal growth restriction. In this study growth restriction was more severe in preterm

Acknowledgements

We acknowledge the skilled technical assistance of Katy Freed, Peter Stebbing, and Dina Tsatas. We thank clinical research nurses Jane Atkinson, Nicola Davies, Linda Horton, and Jenny Robinson and the midwifery and obstetrics staff of the Royal Women’s Hospital for their generous assistance.

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    Supported by the National Health and Medical Research Council of Australia (Jane M. Moseley, PhD, Gregory E. Rice, PhD, and Mary E. Wlodek, PhD) and by Monash University (graduate scholarship to Narelle E. Curtis, PhD).

    ☆☆

    Reprint requests: Mary E. Wlodek, PhD, Department of Physiology, University of Melbourne, Victoria 3010, Australia.

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