Fetus-Placenta-NewbornPreterm fetal growth restriction is associated with increased parathyroid hormone–related protein expression in the fetal membranes☆,☆☆
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).Clinical group No. 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.
References (28)
- et al.
Parathyroid hormone–related protein: a peptide of diverse physiological functions
Trends Endocrinol Metab
(1993) - et al.
Physiological roles for parathyroid hormone–related protein: lessons from gene knockout mice
Vitam Horm
(1996) - et al.
Vascular effects of PTHrP(1-34) in the human fetalplacental circulation
Placenta
(1997) - et al.
Intrauterine growth restriction in infants of less than thirty-two weeks’ gestation: associated placental pathologic features
Am J Obstet Gynecol
(1995) - et al.
Intrauterine growth restriction with absent end-diastolic flow velocity in the umbilical artery is associated with maldevelopment of the placental terminal villous tree
Am J Obstet Gynecol
(1996) - et al.
Comparison of associated high-risk factors and perinatal outcome between symmetric and asymmetric fetal intrauterine growth retardation
Am J Obstet Gynecol
(1991) - et al.
Tumor necrosis factor-α in midtrimester amniotic fluid is associated with impaired intrauterine fetal growth
Am J Obstet Gynecol
(1992) - et al.
Synergistic stimulation of parathyroid hormone–related peptide gene expression by mechanical stretch and angiotensin II in rat aortic smooth muscle cells
J Biol Chem
(1994) - et al.
Parathyroid hormone–related protein
Crit Rev Clin Lab Sci
(1995) - et al.
Defining the roles of the parathyroid hormone–related protein in normal physiology
Physiol Rev
(1996)
Parathyroid hormone–related protein (PTHrP) mRNA splicing and parathyroid hormone/PTHrP receptor mRNA expression in human placenta and fetal membranes
J Mol Endocrinol
Abundant expression of parathyroid hormone–related protein in human amnion and its association with labor
Proc Natl Acad Sci U S A
Parathyroid hormone–related protein mRNA in avascular human amnion
J Clin Endocrinol Metab
The expression of parathyroid hormone related protein mRNA and immunoreactive protein in human amnion and choriodecidua is increased at term compared with preterm gestation
J Endocrinol
Cited by (18)
A key moment for TiO<inf>2</inf>: Prenatal exposure to TiO<inf>2</inf> nanoparticles may inhibit the development of offspring
2020, Ecotoxicology and Environmental SafetyCitation Excerpt :Placenta is one of the crucial protective organs preventing fetus from xenobiotic and infections (Gude et al., 2004), it is also the bridge for exchanging materials between fetus and mother, such as transport of nutrients to the embryo. Dysfunction in placenta can restrict fetal growth, leading to fetal weight loss and increased mortality (Curtis et al., 2000). To date, a systematic overview on the effects of prenatal TiO2 NPs exposure on the development of offspring is lacking.
Production and characterisation of gilthead sea bream (Sparus auratus) recombinant parathyroid hormone related protein
2005, General and Comparative EndocrinologyFetal growth restriction is associated with increased apoptosis in the chorionic trophoblast cells of human fetal membranes
2005, PlacentaCitation Excerpt :As a result, the normal integrity and/or function of the fetal membrane could be impaired and fetal growth consequently restricted. A possible consequence of the significantly increased incidence of apoptosis in the chorionic trophoblast cell layer of FGR-affected fetal membranes may be that production of important proteins and/or factors that regulate fetal growth, for example parathyroid hormone related protein, PTHrP [49–51], interleukin-10 [52] could be affected and this contributes to the etiology of FGR. Elucidation of the molecular mechanisms involved in the control of apoptosis in the chorionic trophoblast layer in the FGR-affected fetal membranes may provide further insight to etiology of FGR.
- ☆
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.