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

FOZZATTI L; VÈLEZ ML; LUCERO AM; NICOLA JP; PELLIZAS CG; ROTH G; MASINI-REPISO AM

JOURNAL OF ENDOCRINOLOGY

Society for Endocrinology

Año: 2007 vol. 192 p. 627 - 627

1479-6805

itric 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-nitroL-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 a