N‐terminal parathyroid hormone‐related protein levels in human intrauterine growth restricted pregnancies

Abstract

The reduced fetal N-terminal parathyroid hormone-related protein concentrations in intrauterine growth restriction may reflect compromised placental function and impaired fetal growth, suggesting that N-terminal parathyroid hormone-related protein may be involved in the pathogenesis of intrauterine growth restriction.

Bone Development and Mineral Homeostasis in the Fetus and Neonate: Roles of the Calciotropic and Phosphotropic Hormones

“…A single study reported that the plasma PTHrP 1-34 level was reduced 50% between birth and day 1 in healthy newborns, but it then increased back to the cord blood level by day 2 (72). As in the animal models, human milk is a very potent source of PTHrP that could support the circulating level if absorbed; by comparison, PTHrP concentrations are low to absent in infant formulas (306,392,488).…”

“…Vesicles prepared from fetal-facing basement membranes of syncytiotrophoblasts (32-37 wk of gestation) showed a linear increase in ATP-dependent accumulation of 45 Ca within the vesicles (649), which is consistent with a progressively increasing rate of active placental calcium transport in late gestation. Mid-molecular PTHrP 38 -94 stimulated ATP-dependent uptake of 45 Ca calcium in a concentration-dependent fashion starting at the physiological dose of 5 pg/ml (648), while PTH, PTHrP , PTHrP [67][68][69][70][71][72][73][74][75][76][77][78][79][80][81][82][83][84][85][86] , and calcitonin had only modest effects at pharmacological doses (50 or 250 pg/ml) (648). 45 Ca uptake was inhibited by a protein kinase C inhibitor, while PTHrP 38 -94 increased inositol tri-sphosphate production and protein kinase C phosphorylation.…”

“…Sixty minutes later, 45 Ca and 51 Cr-EDTA were administered to the mother by intracardiac injection, and the fetuses were removed 30 min after that. PTHrP and PTHrP [67][68][69][70][71][72][73][74][75][76][77][78][79][80][81][82][83][84][85][86] increased the accumulation of 45 Ca/ 51 Cr-EDTA to a value not different from WT littermates, whereas PTH 1-84 and PTHrP had no significant effect (340). Importantly, injections of mid-molecular PTHrP had no effect in WT fetuses, which suggests that the WT fetus may already have maximally stimulated PTHrP responses on the placenta, such that pharmacological treatment had no additional effect.…”

“…Peptides that contained a mid-region portion of PTHrP (PTHrP , PTHrP , and PTHrP [67][68][69][70][71][72][73][74][75][76][77][78][79][80][81][82][83][84][85][86] ) increased the rate of change in the concentration of 45 Ca/ 51 Cr-EDTA in the umbilical vein, whereas PTHrP 1-34 and PTH 1-34 had no effect (6,96,556). When PTHrP 38 -94 was later determined to be the structure of mid-regional PTHrP (490,517), these investigators repeated the experiments and confirmed that PTHrP 38 -94 also significantly increased the rate of placental calcium transport in perfused placentas from previously thyroparathyroidectomized fetal lambs (745).…”