CALCITONIN RECEPTOR MESSENGER-RNA EXPRESSION IN TT CELLS - EFFECT OF DEXAMETHASONE

Citation
Jl. Frendo et al., CALCITONIN RECEPTOR MESSENGER-RNA EXPRESSION IN TT CELLS - EFFECT OF DEXAMETHASONE, Molecular and cellular endocrinology, 139(1-2), 1998, pp. 37-43
Citations number
22
Categorie Soggetti
Endocrynology & Metabolism","Cell Biology
ISSN journal
03037207
Volume
139
Issue
1-2
Year of publication
1998
Pages
37 - 43
Database
ISI
SICI code
0303-7207(1998)139:1-2<37:CRMEIT>2.0.ZU;2-3
Abstract
Among the four isoforms of the calcitonin receptor (CTR) described in humans, two differ by the presence of h-CTR1 or absence of h-CTR2 of 1 6 amino acids in the first intracellular loop. Both receptors are biol ogically active. The TT cell line derived from a human medullary carci noma of the thyroid is characterized by the secretion of large amounts of calcitonin. We have recently shown that this cell line expresses h -CTR2. In the present work we have studied the expression of CTR durin g TT cell proliferation and used dexamethasone to modify calcitonin ex pression in order to establish if an autocrine regulation involving ca lcitonin and its receptor was functional in the TT cells. The expressi on of this receptor and of calcitonin during TT cell proliferation was studied by reverse transcriptase-polymerase chain reaction (RT-PCR). Dexamethasone, a potent inhibitor of TT cell proliferation, levels (da y 6 of culture) specifically increased receptor levels from day 8 onwa rds. CT peptide and CT mRNA levels decreased or were similar during ex perimental time. CTR regulation by glucocorticoids is suggested in TT cells. Autocrine regulation of CTR is also suggested by relation betwe en CT mRNA levels and CTR mRNA. (C) 1998 Elsevier Science Ireland Ltd. All rights reserved.