| Project/Area Number |
08670855
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Pediatrics
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| Research Institution | Chiba University |
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Principal Investigator |
YASUDA Toshiyuki Chiba Univ.Shool of Medicine Lecturer, 医学部, 講師 (00211615)
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| Co-Investigator(Kenkyū-buntansha) |
WATAKI Kunio Chiba Univ.Shool of Medicine Assistant, 医学部, 助手 (80292697)
新美 仁男 千葉大学, 医学部, 教授 (40009147)
南谷 幹史 千葉大学, 医学部, 医員
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| Project Period (FY) |
1996 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥2,500,000 (Direct Cost: ¥2,500,000)
Fiscal Year 1997: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1996: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | Calcium / Calsium-sensing receptor / parathyroid hormone-related peptide / PHT / PHTrP receptor / neonate / PTHrP / 低カルシウム血症 / 高カルシウム血症 |
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| 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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