|
|
The Iodine Group | |
|
Home | Orthoiodosupplementation | Body | Disease | Special | Overviews |
||
|
|
Fozzatti
Endogenous thyrocyte-produced nitric oxide inhibits iodide uptake and thyroid-specific gene expression in FRTL-5 thyroid cellsL Fozzatti, L María Vélez, M Ariel Lucero, P Juan Nicola, D Iván Mascanfroni, R Daniela Macció, G Claudia Pellizas, A Germán Roth and Ana M Masini-Repiso J Endocrinol. 2007 Mar;192(3):627-637. [abstract only]
"Nitric oxide (NO) is a free radical that mediates a wide array of cell functions. It is generated from L-arginine by NO-synthase (NOS). Expression of NOS isoforms has been demonstrated in thyroid cells. Previous reports indicated that NO donors induce dedifferentiation in thyrocytes. However, the functional significance of endogenous thyrocyte-produced NO has not been explored. This work aimed to study the influence of endogenous NO on parameters of thyroid cell function and differentiation in FRTL-5 cells. We observed that treatment with the NOS inhibitor, L-NAME, increased the TSH-stimulated iodide uptake. The TSH-induced NIS and TG mRNA expression was increased after incubation with L-NAME. In transient transfection assays, TSH-stimulated transcriptional activity of NIS and TG promoters was increased by L-NAME. An increment of the TSH- stimulated cell proliferation was observed after NOS inhibition. Similar results were obtained when the action of another NOS inhibitor, L-NMMA, was analysed for most of these studies. The production of NO, which was no detectable in basal conditions, was increased by TSH. Our data provide strong evidence that endogenous NO could act as a negative signal for TSH-stimulated iodide uptake and thyroid specific gene expression as well as proliferation in thyrocytes. These findings reveal a possible new inhibitory pathway in the regulation of thyroid cell function."
|
|
Home | Orthoiodosupplementation | Body | Disease | Special Topics | OverviewsThe Iodine Group | Books | Disclaimers | Contact Us | Search
|
||
