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Synthesis and Regulation of Thyroid Hormones01:20

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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.
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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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Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size...
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The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
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Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
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Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
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Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
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Selenium supplementation modulates apoptotic processes in thyroid follicular cells.

Immacolata C Nettore1, Emma De Nisco1, Silvio Desiderio1

  • 1Dipartimento di Medicina Clinica e Chirurgia, Università degli Studi di Napoli "Federico II", Napoli, 80131, Italy.

Biofactors (Oxford, England)
|March 3, 2017
PubMed
Summary

Selenium supplementation enhances thyroid follicular cell growth and modulates apoptosis pathways. It reduces cell death and may prevent ER-stress-induced apoptosis, offering insights into selenium

Keywords:
Hashimoto's thyroiditisapoptosisautoimmunityselenium

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Area of Science:

  • Molecular Biology
  • Cell Biology
  • Nutritional Science

Background:

  • Selenium (Se) is an essential micronutrient with critical roles in human health.
  • Thyroid function is influenced by various physiological and pathological processes.
  • Understanding selenium's molecular effects on thyroid cells is crucial for its health implications.

Purpose of the Study:

  • To investigate the molecular effects of selenium supplementation on rat thyroid follicular cells (FRTL5).
  • To evaluate selenium's impact on cell growth, mortality, proliferation, and apoptosis.
  • To determine selenium's role in preventing endoplasmic reticulum (ER) stress-induced apoptosis.

Main Methods:

  • Utilized the well-differentiated rat thyroid follicular cell line FRTL5.
  • Assessed cell growth rate, mortality, and proliferation.
  • Analyzed mRNA levels of pro-apoptotic (p53, Bim) and anti-apoptotic (NF-kB, Bcl2) factors.
  • Evaluated ER-stress apoptosis markers, including caspase activity and protein cleavage.

Main Results:

  • Selenium supplementation significantly improved FRTL5 cell growth rate.
  • Selenium reduced the proportion of cell death and modulated key apoptotic gene expression.
  • High doses of sodium selenite (Na-Se) protected cells from tunicamycin-induced ER-stress apoptosis, evidenced by maintained membrane integrity and reduced caspase activity.

Conclusions:

  • Selenium supplementation positively influences thyroid follicular cell growth and survival.
  • Selenium modulates both pro- and anti-apoptotic pathways in thyroid cells.
  • These findings provide molecular evidence for selenium's protective role against ER-stress-induced apoptosis in the thyroid, relevant to its overall physiopathology.