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Titolo:
THE G(2)M ARREST CAUSED BY IODIDE IS UNRELATED TO THE EFFECTS OF IODIDE AT ADENYLATE-CYCLASE
Autore:
SMERDELY P; PITSIAVAS V; BOYAGES SC;
Indirizzi:
ST GEORGE HOSP,DEPT AGED CARE KOGARAH NSW 2217 AUSTRALIA WESTMEAD HOSP,DEPT CLIN ENDOCRINOL WESTMEAD NSW 2145 AUSTRALIA
Titolo Testata:
Thyroid
fascicolo: 4, volume: 5, anno: 1995,
pagine: 325 - 330
SICI:
1050-7256(1995)5:4<325:TGACBI>2.0.ZU;2-H
Fonte:
ISI
Lingua:
ENG
Soggetto:
RAT-THYROID CELLS; FRTL5 CELLS; GROWTH; PROLIFERATION; STIMULATION; CULTURE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
15
Recensione:
Indirizzi per estratti:
Citazione:
P. Smerdely et al., "THE G(2)M ARREST CAUSED BY IODIDE IS UNRELATED TO THE EFFECTS OF IODIDE AT ADENYLATE-CYCLASE", Thyroid, 5(4), 1995, pp. 325-330

Abstract

Previously, we have shown that iodide was able to inhibit TSH inducedthyrocyte proliferation by arresting the cell cycle at G(0)G(1) and G(2)M, suggesting that iodide may be exerting its effects through more than the TSH-adenylate cyclase-cAMP system. To confirm the effects of iodide on the adenylate cyclase (AC) system, forskolin- and dibutyryl-cyclic-AMP (dBcAMP)-stimulated FRTL5 thyroid cells were exposed to inhibitory concentrations of iodide and the resultant effects on the cellcycle were compared to the effects observed with TSH, using flow cytometric DNA analysis. Forskolin stimulated the proliferation of FRTL5 cells in a dose-dependent manner. Cell numbers rose from baseline by 169 +/- 4% to peak at 10 mu M forskolin. Interestingly, 100 mu M forskolin inhibited cell proliferation, causing cell numbers to fall by approximately 50%. Iodide inhibited forskolin-induced proliferation to baseline levels. However, the pattern of cell cycle perturbation was different to that with TSH-stimulated cells. There were no differences in the proportion of cells in G(0)G(1) between forskolin alone and forskolin + NaI, while there was a marked fall in the proportion of cells in S phase, indicating possible partial arrest at G(0)G(1). Furthermore, there was a marked accumulation of cells in G(2)M over and above that found with TSH + NaI, indicating arrest at G(2)M. dBcAMP maximally stimulated cell numbers to rise from baseline by 125% with 1 mM dBcAMP. Again, higher concentrations of the mitogen had an inhibitory effect onproliferation. The addition of NaI inhibited dBcAMP stimulated cell proliferation. However, unlike the effect of NaI on TSH- or forskolin-induced proliferation, there was no G(0)G(1) arrest in the cell cycle. With dBcAMP, there were decreases in the proportion of cells in both G(0)G(1) and S phases with a marked accumulation of cells in G(2)M indicating that the inhibitory effect of iodide is due purely to G(2)M cell cycle arrest. In this study, the requirement of AC activation for the mediation of TSH-induced proliferation has been confirmed. Further, the inhibitory effects of iodide are mediated by at least 2 mechanisms, one AC related and the other independent of the AC system. Iodide caused significant inhibition at G(0)G(1) and G(2)M with cells stimulated by TSH, while in the presence of forskolin, which stimulates the cAMP cascade at the catalytic component of AC, iodide caused little or nocell cycle arrest at G(0)G(1), but induced marked cell cycle arrest at G(2)M. Further, iodide in the presence of dBcAMP, which acts distal to AC, induced only a G(2)M arrest. This indicates that the G(0)G(1) arrest caused by iodide is due to effects at or proximal to the catalytic component of AC while the G(2)M arrest is unrelated to the effects of iodide at AC.

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Documento generato il 20/09/20 alle ore 22:43:10