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Related Concept Videos

Synthesis and Regulation of Thyroid Hormones01:20

Synthesis and Regulation of Thyroid Hormones

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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.
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...
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Functions of Thyroid Hormones01:18

Functions of Thyroid Hormones

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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.
TH is indispensable for the normal development and maturation of the skeletal, muscular, and nervous systems during fetal and childhood growth. It facilitates bone mineral turnover and regulates protein synthesis in developing tissues, contributing significantly to overall growth and...
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Synthesis and Functions of Calcitonin00:51

Synthesis and Functions of Calcitonin

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Calcitonin, a vital polypeptide hormone, regulates calcium levels within body fluids. It is released by the parafollicular cells, also known as C cells, situated in the follicular epithelium of the thyroid gland. Calcitonin responds to fluctuations in blood calcium levels and the influence of gastrointestinal hormones like gastrin and cholecystokinin.
The exact mechanisms by which calcitonin operates in calcium homeostasis remain elusive, but its significance is evident in several vital...
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Reabsorption and Secretion in the DCT and Collecting Duct01:26

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The early phase of the DCT manages the reabsorption of approximately 10-15% of filtered water, 5–10% of filtered sodium, and 5–10% of filtered chloride. This process is facilitated by Na+–Cl− symporters in apical membranes and sodium-potassium pumps, as well as Cl− leakage channels in basolateral membranes. The early DCT also stands out as a site where parathyroid hormone (PTH) stimulates calcium reabsorption, depending on the body's requirements.
The distal...
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Hormones and Bone Tissue01:17

Hormones and Bone Tissue

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The endocrine system produces and secretes hormones, which interact with the skeletal system. These hormones control bone growth, maintain bone once it is formed, and remodel it.
Hormones That Influence Osteoblasts and/or Maintain the Matrix
Several hormones are necessary for controlling bone growth and maintaining the bone matrix. The pituitary gland secretes growth hormone (GH), which, as its name implies, controls bone growth. This happens in several ways: first, it triggers chondrocyte...
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Regulation of Hormone Secretion01:19

Regulation of Hormone Secretion

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Regulation of hormone secretion is a finely tuned orchestration driven by various types of stimuli, encompassing neural, humoral, and hormonal signals. Environmental cues instigate neural stimuli, where action potentials traverse nerve fibers to reach their designated targets. An illustrative scenario is the body's response to stress, wherein the sympathetic nervous system releases epinephrine from the adrenal glands, inducing the well-known 'fight or flight' reaction.
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Related Experiment Video

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Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
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Deiodinase-3 is a thyrostat to regulate podocyte homeostasis.

Shivangi Agarwal1, Kwi Hye Koh1, Nicholas J Tardi1

  • 1Department of Internal Medicine, Rush University, Chicago, IL 60612.

Ebiomedicine
|October 14, 2021
PubMed
Summary

Type 3 deiodinase (D3) protects kidney podocytes from thyroid hormone (T3) injury. Reduced D3 in podocytes leads to nephrotic syndrome (NS), linking thyroid autoimmunity to kidney disease.

Keywords:
D3Graves’ diseasedeiodinasesintegrinkidneypodocytesthyroid

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Area of Science:

  • Endocrinology
  • Nephrology
  • Molecular Biology

Background:

  • Nephrotic syndrome (NS) involves kidney podocyte injury and is linked to thyroid autoimmunity.
  • Thyroid hormone (TH) regulation in podocytes is not well understood.
  • Type 3 deiodinase (D3) inactivates TH and its role in kidney disease is unclear.

Purpose of the Study:

  • Investigate how podocytes handle thyroid hormone (TH).
  • Determine the role of type 3 deiodinase (D3) in podocyte function and kidney disease.
  • Explore the link between thyroid autoimmunity and NS.

Main Methods:

  • Utilized immunofluorescence, qPCR, and D3 knockout mice to study D3 in healthy and injured podocytes.
  • Employed surface plasmon resonance (SPR), co-immunoprecipitation, and Proximity Ligation Assay (PLA) for interaction studies.
  • Assessed podocyte injury markers like foot process effacement and proteinuria.

Main Results:

  • Healthy podocytes predominantly express D3, which is reduced upon injury.
  • D3 mislocalization from the cell membrane to the Golgi and nucleus occurs during podocyte injury.
  • D3 depletion or T3 treatment caused podocyte injury, including foot process effacement and proteinuria.
  • Thyroid stimulating hormone receptor (TSH-R) activation on podocytes also led to injury.

Conclusions:

  • D3 acts as a renoprotective 'thyrostat' in podocytes by minimizing T3-induced integrin activation.
  • Reduced D3 function in podocytes contributes to kidney injury.
  • TSH-R activation by antibodies, seen in Graves' disease, provides a mechanistic link between thyroid disorders and NS.