The acute inhibitory effects of iodide excess on sodium/iodide symporter expression and activity involve the PI3K/Akt signaling pathway

SERRANO-NASCIMENTO C; DA SILVA TEIXEIRA S; NICOLA JP; NACHBAR RT, ; CURI R; MASINI - REPISO AM; NUNES MT

ENDOCRINE SOC

Lugar: Chevy Chase, MD ; Año: 2014 vol. 155 p. 1145 - 1145

odide (I-) is an irreplaceable constituent of thyroid hormones and an important regulator of thyroid function, since high concentrations of I- downregulate NIS expression and function. In thyrocytes, activation of PI3K/Akt cascade also inhibits NIS expression and function. Since I- excess and PI3K/Akt signaling pathway induce similar inhibitory effects on NIS expression, we aimed to study whether the PI3K/Akt cascade mediates the acute and rapid inhibitory effect of I- excess on NIS expression/activity. Here, we reported that the treatment of PCCl3 cells with I- excess increased Akt phosphorylation under normal or TSH/insulin starving conditions. I- stimulated Akt phosphorylation in a PI3K-dependent manner, since the use of PI3K inhibitors (wortmannin or LY294002) abrogated the induction of