1989 Fiscal Year Final Research Report Summary
Synthesis and secretion of calcitonin and calcitonin gene-related peptide.
| Project/Area Number |
63570150
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Human pathology
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| Research Institution | Tokai Univ, School of Medicine |
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Principal Investigator |
KAKUDO K. Tokai Univ. Dept of Pathol. Assist. Prof., 医学部・病理学, 講師 (00112037)
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| Co-Investigator(Kenkyū-buntansha) |
OSAMURA Y. Tokai Univ. Dept of Pathol. Prof., 医学部・病理学, 教授 (10100992)
WATANABE K. Tokai Univ. Dept of Pathol. Prof., 医学部・病理学, 教授 (00055865)
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| Project Period (FY) |
1988 – 1989
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| Keywords | Thyroid Gland / C cell / Calcitonin / Secretion / Cell cycle / Calcium metabolism / GCRP |
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| Research Abstract |
Calcitonin(CT) and calcitonin gene-related peptide(CGRP) are synthesized in and secreted from the C cells of the thyroid. To study regulation mechanism of these peptides, the following studies were carried out and clarified. These 2 peptides are localized in the neurosecretory granules of the human C cells of the thyroid at electron microscopic level. When calcium channel blocker nifedipine was applied on cultured C cells(TT cells), CT secretion in the culture media was reduced and numbers of secretory granules in the TT cells were increased. When synthetic salmon calcitonin (TZ-CT) was injected in rats, tissue CT contents reduced in thyroid markedly. In addition to it, CT-m-RNA in the thyroid dropped at 50-80%. Thus TZ-CT administration suppresses CT-m-RNA translation and CT synthesis. Long term TZ-CT administration in the rats suppressed C cell population in the rats thyroid. This negative feedback mechanism may suggests that C cells may have CT receptors and were regulated CT synthesis and secretion by serum CT levels directly rather than by serum calcium level indirectly.
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