Inhibitory effects of 2-iodohexadecanal on FRTL-5 thyroid cells proliferation
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...
| Autores: | , , , , , , , , |
|---|---|
| Tipo de recurso: | artículo |
| Estado: | Versión publicada |
| Fecha de publicación: | 2015 |
| País: | Argentina |
| Institución: | Consejo Nacional de Investigaciones Científicas y Técnicas |
| Repositorio: | CONICET Digital (CONICET) |
| Idioma: | inglés |
| OAI Identifier: | oai:ri.conicet.gov.ar:11336/180162 |
| Acceso en línea: | http://hdl.handle.net/11336/180162 |
| Access Level: | acceso abierto |
| Palabra clave: | IODINE IODOHEXADECANAL IODOLIPIDS THYROID https://purl.org/becyt/ford/1.6 https://purl.org/becyt/ford/1 |
| Sumario: | 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. |
|---|