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Effects of 17β‐estradiol on calcitonin secretion and content in a human medullary thyroid carcinoma cell line
Author(s) -
LazarettiCastro Marise,
Grauer Andreas,
Mekonnen Yalem,
Raue Friedhelm,
Ziegler Reinhard
Publication year - 1991
Publication title -
journal of bone and mineral research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.882
H-Index - 241
eISSN - 1523-4681
pISSN - 0884-0431
DOI - 10.1002/jbmr.5650061108
Subject(s) - calcitonin , endocrinology , medicine , secretion , forskolin , estrogen , in vivo , cell culture , stimulation , thyroid carcinoma , thyroid , biology , chemistry , genetics , microbiology and biotechnology
Abstract The presence of a direct estrogen effect on calcitonin secretion is controversial. Because most of the data available were obtained from complex in vivo systems, we chose an in vitro approach to assess the problem. Using a human C cell carcinoma cell line (TT cells) with well‐documented estrogen receptors, we investigated the effect of 17β‐estradiol (E 2 ) on basal and stimulated calcitonin secretion, on calcitonin content, and on total cellular protein. After short (30 and 180 minutes) and long‐term (24 h to 6 days) incubation of the cells with different concentrations of E 2 (from 0.01 to 100 nM) we observed no stimulatory but a transient dose‐dependent inhibitory effect on CT secretion and content. The nadir of the effect on CT secretion appeared at 24 h, demonstrating a reduction to 80.5 ± 7.8% of control at 1 nM and to 59.1 ± 15% of control at 100 nM E 2 . After 72 h, the CT levels of the E 2 ‐exposed groups returned to control levels. The acute stimulation of the cells with TPA plus forskolin after preincubation with E 2 up to 6 days showed no difference in the increment of CT release compared to the control groups. Additionally, E 2 had a dose‐dependent stimulatory effect on cell protein content. The data demonstrate the absence of a direct stimulatory effect of E 2 on CT secretion, revealing a dose‐dependent inhibitory effect on CT secretion and content.