S-Nitrosylation of NF-κB p65 Inhibits TSH-Induced Na(+)/I(-) Symporter Expression.

NICOLA JUAN PABLO; PEYRET V.; NAZAR M.; ROMERO JM; LUCERO A.M.; MONTESINOS M.M.; BOCCO J.L.; PELLIZAS C.G.; MASINI-REPISO A.M.

ENDOCRINE SOC

Lugar: Baltimore; Año: 2015 vol. 156 p. 4741 - 4741

itric oxide (NO) is a ubiquitous signaling molecule involved in a wide variety of cellular physiological processes. In thyroid cells, NO-synthase III-endogenously produced NO reduces TSH-stimulated thyroid-specific gene expression, suggesting a potential autocrine role of NO in modulating thyroid function. Further studies indicate that NO induces thyroid dedifferentiation, because NO donors repress TSH-stimulated iodide (I−) uptake. Here, we investigated the molecular mechanism underlying the NO-inhibited Na+/I− symporter (NIS)-mediated I− uptake in thyroid cells. We showed that NO donors reduce I− uptake in a concentration-dependent manner, which correlates with decreased NIS protein expression. NO-reduced I− uptake results from transcriptional repression of NIS gene rather than posttranslational modifications reducing functional NIS expression at the plasma membrane. We observed that NO donors repress TSH-induced NIS gene expression by reducing the tran