Possible direct induction by estrogen of calcitonin secretion from ultimobranchial cells in the goldfish
The plasma level of calcitonin (CT), a calcium (Ca)-regulating hormone, is known to increase in female teleosts during the reproductive period. In the present study, a correlation between plasma CT and Ca and one between plasma CT and the gonad somatic index were demonstrated in the female goldfish...
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Veröffentlicht in: | General and comparative endocrinology 2004-09, Vol.138 (2), p.121-127 |
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Sprache: | eng |
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Zusammenfassung: | The plasma level of calcitonin (CT), a calcium (Ca)-regulating hormone, is known to increase in female teleosts during the reproductive period. In the present study, a correlation between plasma CT and Ca and one between plasma CT and the gonad somatic index were demonstrated in the female goldfish but not in the male. To clarify the relationship between CT and Ca, we examined the plasma CT and Ca levels after injecting immature goldfish with estrogen. At day 1, the plasma CT level significantly increased, whereas the plasma Ca level was not changed from its initial level. This result suggests that the trigger of CT secretion is estrogen and that estrogen directly acts on the ultimobranchial gland (UBG), a CT-secreting organ. To determine whether the UBG is equipped with estrogen receptor (ER), an ER binding assay and immunohistochemical staining of UBG cells with an antibody against ER were conducted. As a result, estrogen-specific binding (
K
d, 18.52
nM;
B
max, 1.35
pmol/mg protein) and ER-immunoreactivity in the UBG were demonstrated. Furthermore, the expression of α,β, and γ types of ER in the UBG was also detected by use of the reverse-transcription polymerase chain reaction. Thus, we concluded that estrogen acts on the UBG to induce the release of CT, which in turn plays an important role in reproduction directly and/or indirectly through Ca. This is the first report on the existence of ERs in a teleost UBG and the occurrence of CT secretion caused by estrogen. |
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ISSN: | 0016-6480 1095-6840 |
DOI: | 10.1016/j.ygcen.2004.05.013 |