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Titolo:
METHIMAZOLE INHIBITS FRTL5 THYROID-CELL PROLIFERATION BY INDUCING S-PHASE ARREST OF THE CELL-CYCLE
Autore:
SMERDELY P; PITSIAVAS V; BOYAGES SC;
Indirizzi:
WESTMEAD HOSP,DEPT CLIN ENDOCRINOL WESTMEAD NSW 2145 AUSTRALIA
Titolo Testata:
Endocrinology
fascicolo: 5, volume: 133, anno: 1993,
pagine: 2403 - 2406
SICI:
0013-7227(1993)133:5<2403:MIFTPB>2.0.ZU;2-N
Fonte:
ISI
Lingua:
ENG
Soggetto:
GROWTH;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
15
Recensione:
Indirizzi per estratti:
Citazione:
P. Smerdely et al., "METHIMAZOLE INHIBITS FRTL5 THYROID-CELL PROLIFERATION BY INDUCING S-PHASE ARREST OF THE CELL-CYCLE", Endocrinology, 133(5), 1993, pp. 2403-2406

Abstract

Previous studies, using tritiated thymidine uptake assays, had indicated a nil or stimulatory effect of methimazole (MMI) on thyroid cell proliferation. Whilst examining cell cycle kinetics of FRTL5 thyrocytes, we observed an inhibitory effect of MMI on thyroid cell proliferation. To further examine this observation, FRTL5 cells whilst in log phase proliferation were exposed to media containing either 6H or MMI in 6H. Cell number and cell cycle kinetics were examined using flow cytometric DNA analysis every 24 hrs for 96 hrs. We found that MMI inhibitedcell proliferation (as assessed by cell number) throughout the experimental period. Cell cycle analysis revealed a persistent arrest of cells in S phase. Concomitantly, there was a fall in the proportion of cells in both GOG1 and G2M phases, in keeping with cell cycle arrest in S phase. Taken in isolation, the finding of a high proportion of cellsin S phase would suggest stimulation of cell proliferation, consistent with the findings of previous studies which used tritiated thymidineuptake assays to assess cell proliferation. However, the absence of aconcomitant increase in total cell number renders this argument invalid and argues for a specific effect of MMI on the cell cycle. This study demonstrates a hitherto unrecognised inhibitory action of MMI on FRTL5 thyroid cell proliferation which has implications in understandingthe broader effects of MMI on thyroid cell physiology. Additionally, this study highlights the dangers of using tritiated thymidine uptake measures as the sole indicator of mitogenic activity.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 20/09/20 alle ore 23:42:37