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Related Concept Videos

Synthesis and Regulation of Thyroid Hormones01:20

Synthesis and Regulation of Thyroid Hormones

Low blood levels of the thyroid hormones — triiodothyronine (T3) and thyroxine (T4) — signal the hypothalamus to release the thyrotropin-releasing hormone (TRH). TRH then reaches the pituitary gland and stimulates the release of thyroid-stimulating hormone(TSH) into the bloodstream.
Upon reaching the thyroid gland, TSH stimulates the follicular cells' active uptake of iodide ions from the blood. The ions diffuse to the apical surface of the cells and are oxidized to iodine. The iodine is then...
TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors are of three kinds RI, RII, and RIII. The RI...
Functions of Thyroid Hormones01:18

Functions of Thyroid Hormones

The thyroid hormone (TH) plays a pivotal role in the intricate orchestration of physiological processes, exerting profound effects on development, metabolism, and homeostasis throughout different life stages.
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Graves Disease II: Pathophysiology01:24

Graves Disease II: Pathophysiology

Graves’ disease is an autoimmune disorder characterized by the production of thyroid-stimulating immunoglobulins (TSI) that activate TSH receptors, leading to excessive synthesis and release of thyroid hormones (T3 and T4) and resulting in hyperthyroidism.Among all causes of hyperthyroidism, Graves’ disease is the most common and can happen at any age, though it is more frequent in women. It produces a hypermetabolic state with features such as weight loss, tachycardia, tremor, and heat...
Hyperthyroidism II: Pathophysiology01:27

Hyperthyroidism II: Pathophysiology

Hyperthyroidism is a hypermetabolic state caused by elevated levels of thyroid hormones, triiodothyronine (T3) and thyroxine (T4). It results from dysregulation at the thyroid, pituitary, or immune system level and affects multiple organ systems.PathophysiologyThe most common cause of hyperthyroidism is Graves’ disease, an autoimmune disorder in which antibodies, specifically thyroid-stimulating antibodies (TSAb), a subtype of TSH receptor antibodies (TRAb), bind to and activate TSH receptors...
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Hyperthyroidism is a type of thyrotoxicosis characterized by the thyroid gland's overproduction of the thyroid hormones triiodothyronine (T3) and thyroxine (T4). This hormone excess increases the basal metabolic rate and enhances sensitivity to catecholamines.DiagnosisDiagnosis is based on clinical features and biochemical testing. It typically shows suppressed thyroid-stimulating hormone (TSH) levels below 0.4 mIU/L, with elevated free T3 and/or T4. Additional tests, including thyroid...

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Related Experiment Video

Updated: Jun 2, 2026

An Ex vivo Culture System to Study Thyroid Development
08:33

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Published on: June 6, 2014

Transforming growth factor beta 1 (TGF-beta 1) expression in proliferating thyroid disease.

E Perlino1, A Ciampolillo, E Maiorano

  • 1UNIV BARI,INST MED ENDOCRINOL & METAB DIS,BARI,ITALY. UNIV BARI,FAC MED,INST PATHOL ANAT,BARI,ITALY. UNIV BARI,FAC SCI,DEPT BIOCHEM & MOLEC BIOL,BARI,ITALY. UNIV MILAN,EUROPEAN INST ONCOL,DEPT PATHOL,MILAN,ITALY.

International Journal of Oncology
|May 5, 2011
PubMed
Summary

Transforming growth factor-beta 1 (TGF-beta 1) expression is significantly altered in thyroid diseases. This study reveals TGF-beta 1

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Area of Science:

  • Endocrinology
  • Molecular Biology
  • Oncology

Background:

  • Thyroid proliferating diseases encompass carcinoma, adenoma, and multinodular goiter.
  • Understanding the molecular pathogenesis of these conditions is crucial for effective treatment.
  • Transforming growth factor-beta (TGF-beta) is implicated in cell growth and differentiation.

Purpose of the Study:

  • To investigate the role of TGF-beta 1 in the pathogenesis of thyroid carcinoma, adenoma, and multinodular goiter.
  • To elucidate the expression patterns and production mechanisms of TGF-beta 1 in these thyroid conditions.

Main Methods:

  • Surgical thyroid tissue samples from patients with multinodular goiter, papillary carcinoma, and follicular adenoma were analyzed.
  • TGF-beta 1 gene expression was evaluated using Northern analysis.
  • Immunocytochemical analysis was performed to determine TGF-beta 1 production sites.

Main Results:

  • TGF-beta 1 gene expression was dramatically increased in malignant thyroid disease (papillary carcinoma) compared to normal thyroid tissue.
  • A significant decrease in TGF-beta 1 expression was observed in multinodular goiter patients relative to normal thyroid.
  • Immunocytochemistry indicated autocrine TGF-beta 1 production in carcinoma and multinodular goiter, and both autocrine and paracrine production in adenoma.

Conclusions:

  • TGF-beta 1 plays a significant role in the molecular mechanisms of thyroid proliferating diseases.
  • Expression levels and production modes of TGF-beta 1 differ between malignant and benign thyroid conditions.
  • These findings support the hypothesis that TGF-beta 1 regulates thyrocyte growth and differentiation in various thyroid pathologies.