Identification of iodinated proteins in cultured thyrocytes and their possible significance for thyroid hormone formation.

The thyroid gland is known to generate the iodinated hormones T3 and T4 from the prohormone thyroglobulin. In this report we examined whether polypeptides other than thyroglobulin are iodinated and hormonogenic in thyrocytes and the prerequisites for their iodination. In primary cultures of porcine thyrocytes, a substantial portion of organified radioiodine was incorporated into cellular proteins other than thyroglobulin. Some of these were identified by immunoprecipitation. They included proteins of the extracellular matrix, plasma membrane proteins, and lysosomal enzymes, which follow in part a secretion and recapture pathway. All of these proteins come into contact with the iodinating system of thyrocytes located on the apical plasma membrane and possess iodination consensus sequences. Immunoprecipitation with T3- or T4-specific antibodies showed that thyroid hormones were detectable only within thyroglobulin. This was confirmed by an analysis of the iodoamino acids of thyroglobulin, cathepsin-D (representing a secretory protein), and aminopeptidase-N (a membrane-integrated protein) by two-dimensional TLC, which revealed the presence of T3 and T4 only within the polypeptide chain of thyroglobulin. These results indicate that iodoproteins other than thyroglobulin do not participate in the generation of thyroid hormones in situ.

Autoregulation of thyroid iodide transport: evidence for the mediation of protein synthesis in iodide-induced suppression of iodide transport.

The role of protein synthesis in iodide-induced suppression of subsequent iodide transport (iodide autoregulation) was studied in cat thyroid slices. Thyroid slices were pretreated for 60-120 min in the presence or absence of either excess (30 microM) sodium iodide, inhibitors of protein synthesis, or both. Tissue was then washed in the presence of 2 mM methimazole to prevent subsequent iodination reaction and remove excess iodide. Iodide transport activity was finally evaluated by measurement of the ratio of tissue to medium iodide concentrations in 90-min incubations. Addition of 0.1 mM cycloheximide during the preexposure of thyroid tissue to excess iodide had no effect on either control levels of iodide transport or iodide-induced autoregulation. However, if thyroid tissue was treated with cycloheximide alone for 1 h before preexposure to excess iodide, there was a significant reduction in the degree of iodide-induced induced autoregulation. Similar results were obtained with pretreatment of the tissue with 0.5 mM puromycin and 1 microgram/ml emetine. These findings suggest that protein synthesis is involved in the mechanism of thyroid autoregulation of iodide transport. Cycloheximide had no effect on the ability of excess iodide to reduce TSH-stimulated cAMP formation. Two-dimensional gel electrophoresis-isoelectric focusing and Sephadex G-25 column chromatography employing dual-isotope comparison of iodoprotein labeling of control and cycloheximide-treated tissue suggest that the ability of cycloheximide to suppress iodide-induced autoregulation is associated with the reduced iodination of an 8- to 10-kilodalton soluble component of the thyroid gland.

Respuesta de tirotropina (TSH) e iodo unido a proteína (PBI) a stress emocional / Thyrotropin (TSH) and protein bound iodine (PBI) response to emotional stress

Se estudió el efecto de dos tipos diferentes de estrés emocional inducido por estimulación audiovisual sobre las concentraciones de TSH y PBI en sujetos sanos. Con este fin se utilizaron 2 grupos experimentales de 15 y 12 sujetos, con los cuales se efectuaron dos experimentos de metodologías similares y con diferentes estímulos emocionales. En el experimento 1 el estrés se producía por material fílmico inductor de reacciones emocionales negativas y en el experimento II se inducía excitación emocional agradable por estimulación musical. El PBI aumentó significativamente p<0,05 en ambos experimentos y la TSH aumentó significativamente en el primero p<0,05 y no así en el segundo. No se obtuvo correlación significativa entre los incrementos de TSH y sus respectivos incrementos de PBI en el experimento I. Se discute la posibilidad de que las respuesta inespecífica de aumento de PBI sea debida a excitación del sistema nervioso simpático a través de su inervación en los folículos del tiroides, y que la TSH sea susceptible de liberarse selectivamente ante estímulos emocionales específicos(AU)