| Research Abstract |
The parathyroid hormone and 1,25-dihydroxyvitamin D are principle hormones to raise serum calcium levels, and the control of serum calcium around 8.5-10 mg/dl is mainly achieved by the parathryoid calcium-sensing receptor to control parathryoid hormone secretion in man. However, during fetal life, the fetus receives calcium and phosphorus from mother, and consequently the role of parathyroid hormone and 1,25-dihydroxyvitamin D to maintain fetal hypercalcemia may be minor. We do not know the reason why the fetus maintain hypercalcemia. The aim of present study is to elucidate the role of parathyroid hormone-related peptide and the role of parathyroid calcium-sensing receptor and placenta calcium-sensing receptor during fetal and neonatal adaptation. For this porpose, analysis of Jansen metaphyseal chondrodysplasia with hypercalcemia and familial hypoparathyroidism identified during neonatal period was also performed. Parathyroid hormonerelated peptide concentration in cord blood was high which may contribute to a reduction in urine Caexcretion in fetal and early neonatal life. We revealed that a constitutive activation of parathyroid calcium-sensing receptor is a cause of severe familial hypoparathyroidism identified during neonatal period, which may indicate the role of parathyroid calcium-sensing receptor to maintain serum calcium level during perinatal period. Analysis of Jansen metaphyseal chondrodysplasia with hypercalcemia, which cause is constitutive activation of the PTH/PTHrP receptor, suggests that the expression of PTH/PTHrP receptor during fetal life may be low. Therefore, we have examined the level of the PTH/PTHrP receptor mRNA during fetal life. We have also identified that both placental calcium-sensing receptor and parathyroiod hormone-related protein are expressed in cytotrophoblast primary culture cell, however further study is required to elucidate their significance.
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