Endogenous thyrocyte-produced nitric oxide inhibits iodide uptake and thyroid-specific gene expression in FRTL-5 thyroid cells.

FOZZATTI LAURA; VELEZ MARIA LAURA; LUCERO ARIEL MAXIMILIANO; NICOLA JUAN PABLO; MASCANFRONI IVAN DARIO; MACCIO DANIELA RITA; PELLIZAS CLAUDIA GABRIELA; ROTH GERMAN; MASINI-REPISO ANA MARIA

BIOSCIENTIFICA LTD

Año: 2007 vol. 192 p. 627 - 627

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, Nu-nitro-L-arginine methyl ester (L-NAME), increased the TSHstimulated iodide uptake. The TSH-induced sodium iodide symporter (NIS) and thyroglobulin (TG) mRNA expressions were increased after incubation with L-NAME. In transient transfection assays, TSH-stimulated transcriptional activities of NIS and TG promoters were increased by L-NAME. An increment of the TSH-stimulated cell proliferation was observed after NOS inhibitio