Endocrine Abstracts

TSH is the main regulator of the thyroid hormones (THs) synthesis/secretion, which in turn exert a negative feedback mechanism on the Tshb mRNA expression in the pituitary gland by reducing their transcription rate. Some of triiodothyronine (T₃) effects are also shown in short period of time, characterizing the non genomic actions of THs. It has been shown previously that T₃ acts on posttranscriptional steps of TSH synthesis and reduces its secretion when acutely administered to hypothyroid rats. The present study aimed to: i) characterize the pathways involved in the rapid inhibition of the TSH secretion induced by T₃ in primary cultures of anterior pituitary cells and ii) evaluate the participation of T₃ on calcium and magnesium intracellular mobilization in slices of pituitary of hypothyroid rats. The cultured plates were treated with three different stimuli, RGD (100 μg/ml – 50 min), Wortmannin (1 μM – 30 min), and EGTA (1 mM). Lately, T₃ was added (10⁻⁸ M) for 30 min. Slices of pituitary were incubated with Fluo-4AM and Magnesium Green AM probes to address the mobilization of calcium and magnesium after T₃ treatment. The results showed a rapid increase of TSHB content in intracellular extracts while the amount of TSH in extracellular media was reduced after T₃ challenge. The treatment with RGD and Wortmannin abolished T₃ effects. No alteration on TSH secretion induced by T₃ was observed in the presence of EGTA in the culture media neither in calcium intracellular mobilisation, while intracellular concentration of magnesium was altered under the same condition T₃ treatment (16% of pituitary cells). The Therefore, we propose the existence of an additional mechanism that decreases the TSH synthesis/secretion, triggered in few minutes by T₃, through its interaction with αVβ3 integrin at the plasma membrane, featuring a non genomic action of this thyroid hormone on its own synthesis/secretion.

Disclosure: This work was supported by the FAPESP (São Paulo Research Foundation) (2009/17813-9).