Stimulation of calcitonin/CGRP-I and CGRP-II gene expression by dibutyryl cAMP in a human medullary thyroid carcinoma (TT) cell line

Wind, Jobien C.; Born, Walter; Rijnsent, Annemiek; Boer, Pieter; Fischer, Jan A.

doi:10.1016/0303-7207(93)90071-q

Cited by 8 publications

(5 citation statements)

References 28 publications

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“…In these cells, activation of the PKA system with cAMP‐enhancing agents leads to cell growth inhibition and to increased levels of nuclear precursor RNAs for CT and CGRP to the same extent. However, in response to 1 mM (Bu) 2 cAMP, a larger increase in CT secretion was reported compared with that of CGRP, suggesting a modification of the alternative RNA processing of the CT/CGRP transcript 47 . Control of gene expression by cAMP involves activation, through phosphorylation by cAMP‐dependant protein kinase, of specific transcription factor(s) that can bind to the promoter of CT/CGRP gene and then stimulate transcription.…”

Section: Discussionmentioning

confidence: 99%

“…However, in response to 1 mM (Bu) 2 cAMP, a larger increase in CT secretion was reported compared with that of CGRP, suggesting a modification of the alternative RNA processing of the CT/CGRP transcript. (47) Control of gene expression by cAMP involves activation, through phosphorylation by cAMP-dependant protein kinase, of specific transcription factor(s) that can bind to the promoter of CT/CGRP gene and then stimulate transcription. cAMP responsive element (CRE) consensus sequences have been identified in the 5Ј-flanking DNA of the CT/CGRP gene.…”

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confidence: 99%

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Expression of the CT/CGRP Gene and Its Regulation by Dibutyryl Cyclic Adenosine Monophosphate in Human Osteoblastic Cells

Drissi

Hott

Marie

et al. 1997

Journal of Bone and Mineral Research

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Expression of the CT/CGRP Gene and Its Regulation by Dibutyryl Cyclic Adenosine Monophosphate in Human Osteoblastic Cells

Drissi

Hott

Marie

et al. 1997

Journal of Bone and Mineral Research

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“…Cell culture medium was collected and treated as previously described (Wind et al, 1993) (Lamari et al, 1994), an increase in (table I) in comparison to the dexamethasone group. On day 6 of treatment, 5 x 10-6 mol/I alltrans-retinoic acid clearly decreased the release of both CT and CGRP (figs 1 and 2).…”

Section: Other Methodsmentioning

confidence: 99%

Effects of 17β-estradiol on calcitonin and calcitonin-gene-related peptide secretions and contents in a murine medullary thyroid carcinoma C-cell line (CA-77)

Lamari

Ghorbel²,

Jm³

1995

Reprod. Nutr. Dev.

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Summary ― The effect of 17!-estradiol on calcitonin (CT) and calcitonin-gene-related peptide (CGRP) secretions in the murine CA-77 C cell line was studied after 1, 3, 5 and 6 d of treatment. The release of both CT and CGRP significantly increased 1, 3, 5 and 6 d after addition of 0.1 Ilmol/l estradiol alone to the culture medium. The C cell content of both peptides also increased after 6 d of treatment with the same dose of estrogen. The enhanced CT and CGRP secretions induced by 17(3-estradiol were not inhibited by the simultaneous addition of 5 wmol/I of all-trans-retinoic acid. Dexamethasone alone increased the release of both peptides within 6 d. However, when cells were treated simultaneously with estradiol and 1 pmol/I dexamethasone, the addition of retinoic acid blunted both the CT and CGRP secretions induced by dexamethasone. These results showed that the positive effects of 17(3-estradiol on both CT and CGRP secretions were modulated by dexamethasone and retinoic acid.CT secretion / CGRP secretion / CA-77 C cell / 17(3-estradiol / dexamethasone / retinoic acid Résumé ― Le 17p-oestradiol à la dose de 100 nmolll augmente la sécrétion et le contenu cellulaire de CT et de CGRP par la lignée de cellules C (CA-77) d'origine murine. Les effets de /'œsfrad/o/ sur la libération de CT et de CGRP dans le milieu de culture sont observés 1, 3, 5 et 6 j après addition du stéroïde. Le contenu cellulaire en hormones est également légèrement augmenté sous cestradiol. L'acide rétinoi'que all-trans 5 wmolll ne diminue la sécrétion des 2 peptides qu'au bout de 6 j, alors que la dexaméthasone 1 pmolll, seule, stimule la sécrétion de CT et CGRP tout au long du traitement (de 1 à 6 j). Si l'acide rétinoïque n affecte pas le contenu cellulaire en CT et CGRP, la dexaméthasone, en revanche, l'augmente. Le co-traitement par l'c!stradiol et l'acide rétinoique n'inhibe pas l'effet du sté-roïde sur la sécrétion de CT et de CGRP. Dans le cas d'un co-traitement par la dexaméthasone et l'oestradiol, un effet additif n'est observé qu'après 3 j de traitement. Le traitement simultané des cellules C par les 3 molécules montre à chaque fois (1, 3, 5 et

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“…Interestingly, enhancer element binding activities were only found in CT expressing TT-cells, but not in non-expressing HeLa cells (Monla et al, 1995). Furthermore, a direct stimulatory effect of dibutyryl-cAMP on CT gene expression has been demonstrated (Wind et al, 1993). Our interest was in the receptor availability for the adenylyl cyclase system in vitro in long-term culture.…”

Section: Discussionmentioning

confidence: 99%

cAMP-synthesis in a medullary thyroid carcinoma cell line: Response to adrenergic agents and Prostaglandines

Mertens¹,

Goretzki²,

Keck³

2009

Exp Clin Endocrinol Diabetes

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Calcitonin secretion by C-cells is mediated through intracellular 3'5'-cyclic adenosine monophosphate (cAMP) and calcium signaling. Calcitonin release stimulation tests may take advantage of both signaling cascades in screening for medullary thyroid carcinomas (MTC). To elucidate the regulation of the adenylyl cyclase system we have determined cAMP levels of a calcitonin-expressing MTC cell line (RG) after exposure to adrenergic agents and prostaglandines. In early passages (20-30) cAMP concentrations were significantly elevated in RG cells after exposure to beta-adrenergic agents and prostaglandines E1 and E2. In advanced passages (60-80) the beta-adrenergic response was no longer detectable and adrenergic receptors were uncoupled from the adenylyl cyclase complex; while the effect of prostaglandines E1 and E2 remained unaffected. Preincubation with dexamethasone, in a process requiring protein new synthesis, re-established the adrenergic response in later passages, indicating that RG cells dedifferentiated in culture over time. Our in vitro findings suggest that MTC cell dedifferentiation may be accompanied by adrenergic receptor-uncoupling from the adenylate cyclase system and that this process may be reversed by dexamethasone incubation.

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Stimulation of calcitonin/CGRP-I and CGRP-II gene expression by dibutyryl cAMP in a human medullary thyroid carcinoma (TT) cell line

Cited by 8 publications

References 28 publications

Expression of the CT/CGRP Gene and Its Regulation by Dibutyryl Cyclic Adenosine Monophosphate in Human Osteoblastic Cells

Expression of the CT/CGRP Gene and Its Regulation by Dibutyryl Cyclic Adenosine Monophosphate in Human Osteoblastic Cells

Effects of 17β-estradiol on calcitonin and calcitonin-gene-related peptide secretions and contents in a murine medullary thyroid carcinoma C-cell line (CA-77)

cAMP-synthesis in a medullary thyroid carcinoma cell line: Response to adrenergic agents and Prostaglandines

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