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 GERMAN A.; MASINI-REPISO ANA M.

Society for Endocrinology

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

p style="LINE-HEIGHT: normal; MARGIN: 0cm 0cm 10pt; mso-margin-top-alt: auto; mso-margin-bottom-alt: auto" class="MsoNormal">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-induc