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

FOZZATTI L, VÉLEZ ML., LUCERO AM, NICOLA JP., MASCANFRONI, ID., MACCIÓ DR., PELLIZAS CG., ROTH GA., MASINI-REPISO AM

JOURNAL OF ENDOCRINOLOGY

Stanford University Libraries

Lugar: Bristol, United Kingdom; Año: 2006

0022-0795

font face="Helvetica"> 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 actio