Thyroid hormone induction of actin polymerization in somatotrophs of hypothyroid rats: potential repercussions in growth hormone synthesis and secretion.

Thyroid hormone was shown to induce actin cytoskeleton polymerization in hypothyroid astrocytes and osteoblastic cells by a nongenomic mechanism. Polyadenylation of GH mRNA, a process that depends on cytoskeleton-associated proteins, was also shown to be regulated by thyroid hormone. Here we investigated by histochemistry and immunohistochemistry whether acute (100 microg per 100 g body weight, iv, for 30 min) or chronic (5 microg per 100 g body weight, ip, 5 d) administration of T3 to thyroidectomized (Tx) and sham-operated rats affects the somatotrophs F-actin cytoskeleton arrangement and its potential repercussion on GH synthesis and secretion. Thyroidectomy dramatically decreased the amount of somatotrophs F-actin content and induced the disassembly of the actin cytoskeleton. These effects were reversed by acute and chronic administration of T3. In addition, in Tx rat somatotrophs, GH labeling was detected mostly at the cell periphery. After 30 min of T3 administration, GH labeling decreased at periphery and increased in the perinuclear region, suggesting that GH secretion and synthesis were stimulated by T3. No differences were detected in the total actin protein content, although a decrease in the F- and increase in G-actin contents were detected in Tx rat pituitaries, a panorama that was reversed by acute T3 treatment, as shown by Western blotting analysis. The sham-operated animals' somatotrophs were only mildly affected by acute T3 administration. The results indicate that the T3-induced rapid alterations on somatotroph actin cytoskeleton and GH cellular distribution resulted from actin filaments rearrangement, which characterizes a nongenomic action.