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Related Concept Videos

The Parathyroid Glands00:59

The Parathyroid Glands

The two pairs of parathyroid glands embedded within the posterior surface of the thyroid gland are restricted by a dense capsule around them. These glands comprise two distinct cell populations—parathyroid oxyphil and parathyroid principal cells- pivotal in calcium homeostasis.
Oxyphil cells, whose functions remain elusive, emerge during late puberty, adding a layer of complexity to the parathyroid gland's intricacies. In contrast, principal parathyroid cells undertake a vital role by producing...
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Hypothyroidism II: Pathophysiology

Hypothyroidism is a disorder characterized by insufficient production of thyroid hormones, which regulate metabolism, energy balance, and multiple organ systems.TypesHypothyroidism is classified based on the level of dysfunction. Primary hypothyroidism results from intrinsic thyroid gland dysfunction, causing reduced hormone production despite normal or increased stimulation. Secondary hypothyroidism arises from inadequate thyroid-stimulating hormone (TSH) secretion by the pituitary. Tertiary...
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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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Hormones That Influence Osteoblasts and/or Maintain the Matrix
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Enzyme-linked receptors are cell-surface receptors acting as an enzyme or associating with an enzyme intracellularly. They make excellent drug targets. Drugs can bind to the extracellular ligand-binding domain or directly affect their enzymatic domain and alter their activity.
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Hyperthyroidism I: Introduction01:25

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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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Two Techniques to Create Hypoparathyroid Mice: Parathyroidectomy Using GFP Glands and Diphtheria-Toxin-Mediated Parathyroid Ablation
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Prolactin receptor in primary hyperparathyroidism--expression, functionality and clinical correlations.

Felix Haglund1, Ming Lu, Vladana Vukojević

  • 1Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden. Felix.Haglund@ki.se

Plos One
|May 19, 2012
PubMed
Summary

The prolactin receptor (PRLr) is highly expressed in parathyroid tumors, with altered isoforms and localization. Prolactin stimulation impacts gene pathways and PTH secretion, suggesting a role for PRLr in parathyroid adenomas.

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Area of Science:

  • Endocrinology
  • Molecular Biology
  • Oncology

Background:

  • Primary hyperparathyroidism (PHPT) is more common in women, hinting at hormonal influences.
  • The prolactin receptor (PRLr) is implicated in various tumors, prompting investigation in parathyroid tissue.

Purpose of the Study:

  • To investigate the expression and functionality of the prolactin receptor (PRLr) in parathyroid tumors.
  • To explore the potential role of PRLr in the development of parathyroid adenomas.

Main Methods:

  • PRLr expression analysis in 37 sporadic parathyroid tumors and normal parathyroid tissue.
  • In vitro studies using cultured human parathyroid tumor cells to assess PRLr functionality.
  • Gene expression profiling to analyze signaling pathway changes upon prolactin stimulation.

Main Results:

  • High PRLR gene transcripts and PRLr protein (60/70 kDa isoforms) were found in parathyroid tumors.
  • Altered PRLr subcellular localization (cytoplasm, granulae, membrane, lysosomes) was observed in tumors compared to normal tissue.
  • Prolactin stimulation in vitro increased PTH secretion and altered gene transcription in JAK/STAT, RIG-I like receptor, and Type II interferon pathways. PRLR gene expression inversely correlated with plasma calcium levels.

Conclusions:

  • The prolactin receptor is abundant in parathyroid tissue, with altered expression and localization in tumors.
  • PRLr responsiveness to prolactin involves PTH secretion and significant changes in key signaling pathways.
  • These findings suggest a potential role for the prolactin receptor in the pathogenesis of parathyroid adenomas.