Endogenous Thyrocyte-produced Nitric Oxide Inhibits Iodide Uptake and Thyroid-Specific Gene Expression in FRTL-5 Thyroid Cells

FOZZATTI LAURA; VÉLEZ MARÍA L.; LUCERO ARIEL M; NICOLA JUAN P; MASCANFRONI IVÁN D; MACCIÓ DANIELA R; PELLIZAS CLAUDIA G; ROTH GERMÁN A ; MASINI - REPISO ANA M

BIOSCIENTIFICA LTD

Lugar: Londod; Año: 2007 vol. 192 p. 627 - 627

p>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, Nomega-nitro-L-arginine methyl ester (L-NAME), increased the TSH-stimulated 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 inhibiti