2003 Fiscal Year Final Research Report Summary
Pathogenesis and control of renal osteodystrophy
| Project/Area Number |
14571030
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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 |
Kidney internal medicine
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| Research Institution | Wakayama Medical University |
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Principal Investigator |
AKIZAWA Tadao WAKAYAMA MEDICAL UNIVERSITY, MEDICAL DEPARTMENT, PROFESSOR, 医学部, 教授 (40102339)
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| Co-Investigator(Kenkyū-buntansha) |
SAKAGUCHI Toshifumi WAKAYAMA MEDICAL UNIVERSITY, MEDICAL DEPARTMENT, ASSISTANT PROFESSOR, 医学部, 助手 (70343423)
OGATA Hiroaki SYOWA UNIVERSITY, MEDICAL DEPARTMENT, ASSISTANT PROFESSOR, 医学部, 助手 (30296959)
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| Project Period (FY) |
2002 – 2003
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| Keywords | RENAL OSTEODYSTROPHY / SECONDARY HYPERPARATHYROIDISM / PARATHYROID HORMONE / ACTIVE VITAMIN D / CALCIUM SENSING RECEPTOR / VITAMIN D RECEPTOR / CALCIMIMETICS / APOPTOSIS |
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| Research Abstract |
In uremic rats with secondary hyperparathyroidism, following results were observed.
1.Gene expression and protein content of vitamin D receptor (VDR) and calcium sensing receptor (CaR) in parathyroid cell were decreased according to the progression of parathyroid proliferation.
2.Cell proliferation preceded the decrease in CaR.
3.Direct injection of vitamin D analogue in parathyroid gland upregulated decreased CaR and VDR, and suppressed the proliferation of parathyroid cells and induced apoptosis of cells.
4.In advanced secondary hyperparathyroidism, CaR agonist (calcimimetics) suppressed proliferation of cells and upregulated VDR and CaR in parathyroid gland.
5.CaR agonist decreased weight of parathyroid gland.
6.Same findings were also observed by direct injection of vitamin D analogue.
These results elucidated the mechanism by which direct injection of vitamin D analogue into parathyroid and CaR agonist regress the advanced secondary hyperparathyroidism.
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