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Preterm fetal growth restriction is associated with increased parathyroid hormone-related protein expression in the
N E Curtis1, R G King, J M Moseley
1Department of Perinatal Medicine, Royal Women's Hospital, Carlton, Australia.
Insights
Parathyroid hormone-related protein (PTHrP) expression increased in fetal membranes of preterm growth-restricted fetuses. This suggests PTHrP may play a role in the development of preterm fetal growth restriction.
Area of Science:
- Reproductive biology
- Endocrinology
- Fetal development
Background:
- Parathyroid hormone-related protein (PTHrP) is vital for normal fetal growth, placental function, and vascular tone.
- These critical functions are often impaired in fetuses experiencing growth restriction.
- Understanding PTHrP's role in fetal growth restriction is crucial for identifying potential therapeutic targets.
Purpose of the Study:
- To investigate whether intrauterine parathyroid hormone-related protein (PTHrP) expression is elevated in cases of fetal growth restriction.
- To determine if PTHrP levels differ between preterm and term fetal growth restriction.
Main Methods:
- Examined PTHrP messenger ribonucleic acid (mRNA) and protein expression in placental, amnion, and chorion-decidua tissues.
- Utilized Northern blot for mRNA abundance and radioimmunoassay for protein content.
- Compared tissues from women with idiopathic fetal growth restriction (preterm and term) against gestation-matched controls.
Main Results:
- PTHrP mRNA expression was significantly increased in the amnion of preterm growth-restricted fetuses.
- Both PTHrP mRNA and protein levels were elevated in the chorion-decidua of preterm growth-restricted fetuses.
- No significant changes in PTHrP expression were observed in term fetal growth restriction.
Conclusions:
- Elevated PTHrP expression in fetal membranes is associated with preterm, but not term, fetal growth restriction.
- These findings suggest a potential role for PTHrP in the pathogenesis of preterm fetal growth restriction.
- Further research is warranted to elucidate the precise mechanisms of PTHrP involvement.
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.