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Cellular mechanism of action of thyroid hormones
I Di Liegro1, G Savettieri, A Cestelli
1Dipartimento di Biologia Cellulare e dello Sviluppo, Università degli Studi, Palermo, Italy.
Abstract:
It has emerged in the last decade that the molecular mechanism of action of thyroid hormones resembles that of steroids; thyroid hormones indeed exert their effects mainly by directly regulating gene expression, on association with specific chromatin-bound receptors. Of the two thyroid hormones, thyroxine (T4) appears to be a sort of prohormone, whereas triiodothyronine (T3) seems to be the active form; in this respect, T4-deiodination, which occurs at the level of the target tissues, may be crucial in the local homeostasis of T3. Moreover, many cellular compartments, other than the nucleus, can bind thyroid hormone, and at least some of these further sites might play some role in modulating T3 supply to the nucleus. The binding of the T3-receptor complex to chromatin is likely to regulate the structural organization of specific genes and, in some instances, of the chromatin as a whole.
Insights
Thyroid hormones, like steroids, regulate gene expression via chromatin-bound receptors. The active form, triiodothyronine (T3), is crucial for cellular function, with thyroxine (T4) acting as a prohormone.
Area of Science:
- Molecular Endocrinology
- Gene Regulation
Background:
- Thyroid hormones (THs) function similarly to steroid hormones by directly regulating gene expression.
- Thyroxine (T4) acts as a prohormone, while triiodothyronine (T3) is the active form.
- TH action involves binding to specific chromatin-bound receptors.
Purpose of the Study:
- To elucidate the molecular mechanism of thyroid hormone action.
- To highlight the role of T4-deiodination in local T3 homeostasis.
- To explore the significance of extranuclear binding sites for thyroid hormones.
Main Methods:
- Review of molecular mechanisms of thyroid hormone action.
- Analysis of gene expression regulation by thyroid hormone-receptor complexes.
- Investigation of extranuclear binding sites and their potential roles.
Main Results:
- Thyroid hormone action is mediated by direct gene expression regulation through receptor binding to chromatin.
- T4 is converted to the active T3 form in target tissues, influencing local T3 homeostasis.
- Extranuclear binding sites for thyroid hormones may modulate T3 supply to the nucleus.
Conclusions:
- The T3-receptor complex binding to chromatin regulates specific gene structures and potentially overall chromatin organization.
- Understanding thyroid hormone action provides insights into endocrine system regulation and gene expression control.