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Войти в исследования Molecular and cellular endocrinology · 2015
Inhibitory effects of 2-iodohexadecanal on FRTL-5 thyroid cells proliferation.
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Thomasz Lisa, Coulonval Katia, Salvarredi Leonardo, Oglio Romina, Fusco Alfredo, Rossich Luciano, Pisarev Mario A, Roger Pierre P, Juvenal Guillermo J
Аннотация
UNLABELLED: Although thyroid gland function is mainly under the control of pituitary TSH, other factors, such as iodine, play a role in this process. The thyroid is capable of producing different iodolipids such as 6-iodo-deltalactone and 2-iodohexadecanal (2-IHDA). It was shown that these iodolipids mimic some of the inhibitory effects of excess iodide on several thyroid parameters.
OBJECTIVES: To study the effect of 2-IHDA on cell proliferation and apoptosis in FRTL-5 cells.
RESULTS: FRTL-5 cells were grown in the presence of TSH and treated with increasing concentrations of KI and 2-IHDA (0.5, 5, 10 and 33 µM) for 24, 48 and 72 h. Whereas KI inhibited cell proliferation only at 33 µM after 72 h of treatment, 2-IHDA inhibited in a time and concentration dependent manner. Analysis of cell cycle by flow cytometric DNA analysis revealed an accumulation of cells in G1 phase induced by 2-IHDA. The expression of cyclin A, cyclin D1 and cyclin D3 were reduced after treatment with 2-IHDA whereas CDK4 and CDK6 proteins were not modified. 2-IHDA induced a dynamic change in cytoplasmic to nuclear accumulation of p21 and p27 causing these proteins to be accumulated mostly in the nucleus. We also observed evidence of a pro-apoptotic effect of 2-IHDA at highest concentrations. No significant effect of KI was observed.
CONCLUSION: These results suggest that the inhibitory effects of 2-IHDA on FRTL-5 thyroid cell proliferation are mediated by cell cycle arrest in G1/S phase and cell death by apoptosis.
OBJECTIVES: To study the effect of 2-IHDA on cell proliferation and apoptosis in FRTL-5 cells.
RESULTS: FRTL-5 cells were grown in the presence of TSH and treated with increasing concentrations of KI and 2-IHDA (0.5, 5, 10 and 33 µM) for 24, 48 and 72 h. Whereas KI inhibited cell proliferation only at 33 µM after 72 h of treatment, 2-IHDA inhibited in a time and concentration dependent manner. Analysis of cell cycle by flow cytometric DNA analysis revealed an accumulation of cells in G1 phase induced by 2-IHDA. The expression of cyclin A, cyclin D1 and cyclin D3 were reduced after treatment with 2-IHDA whereas CDK4 and CDK6 proteins were not modified. 2-IHDA induced a dynamic change in cytoplasmic to nuclear accumulation of p21 and p27 causing these proteins to be accumulated mostly in the nucleus. We also observed evidence of a pro-apoptotic effect of 2-IHDA at highest concentrations. No significant effect of KI was observed.
CONCLUSION: These results suggest that the inhibitory effects of 2-IHDA on FRTL-5 thyroid cell proliferation are mediated by cell cycle arrest in G1/S phase and cell death by apoptosis.