Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Pathophysiology of primary hyperparathyroidism.

P Hellman1, T Carling, L Rask

  • 1Department of Surgery, Uppsala University, Sweden. per.hellman@kirurgi.uu.se

Histology and Histopathology
|May 16, 2000
PubMed
Summary

Parathyroid hormone (PTH) release is regulated by calcium-sensing receptors (CaR) and megalin on parathyroid cells. Dysregulation in hyperparathyroidism involves reduced expression of these receptors and altered calcium sensitivity.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Is allograft rejection a clue to the mechanism promoting MHC polymorphism?

Immunology today·2014
Same author

Variable p-glycoprotein immunoreactivity unrelated to cytotoxic drug-resistance in-vitro of human adrenocortical carcinoma.

International journal of oncology·2011
Same author

Oncolytic adenovirus modified with somatostatin motifs for selective infection of neuroendocrine tumor cells.

Gene therapy·2011
Same author

The myrosinase-glucosinolate system in the interaction between Leptosphaeria maculans and Brassica napus.

Molecular plant pathology·2010
Same author

Neuroendocrine gastroenteropancreatic tumours: ESMO Clinical Practice Guidelines for diagnosis, treatment and follow-up.

Annals of oncology : official journal of the European Society for Medical Oncology·2010
Same author

Stathmin as a marker for malignancy in pheochromocytomas.

Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association·2009

Area of Science:

  • Endocrinology and Calcium Homeostasis
  • Molecular Biology of Hormone Regulation

Background:

  • The parathyroid gland regulates systemic calcium homeostasis via parathyroid hormone (PTH) release.
  • Calcium-sensing receptors (CaR) on parathyroid cells inversely regulate PTH secretion in response to extracellular calcium.
  • Familial hypocalciuric hypercalcemia (FHH) results from inherited inactivation of the CaR.

Purpose of the Study:

  • To review the regulation of PTH release and its dysregulation in hyperparathyroidism (HPT).
  • To explore the roles of CaR and megalin in parathyroid cell function and calcium sensing.
  • To discuss potential contributing factors to HPT, including genetic disturbances and vitamin D deficiency.

Main Methods:

  • Review of existing literature on parathyroid gland physiology and pathology.

Related Experiment Videos

  • Analysis of data concerning calcium-sensing receptors (CaR) and megalin expression and function.
  • Examination of genetic factors and hormonal influences (e.g., vitamin D) in HPT.

    • Main Results:

    • Hyperparathyroidism (HPT) is characterized by excessive PTH secretion and reduced cellular calcium sensitivity (rightward shift of the set-point).
    • Pathological parathyroid cells exhibit decreased expression of both CaR and megalin, and reduced intracellular lipids.
    • Multifactorial genetic disturbances contribute to HPT; reduced vitamin D effect is a potential factor, especially in postmenopausal women.

    Conclusions:

    • CaR and megalin are crucial for normal PTH regulation; their reduced expression is implicated in HPT.
    • Vitamin D deficiency, influenced by age, environment, and genetics (VDR haplotype), may play a role in HPT pathogenesis.
    • Understanding these regulatory mechanisms and dysfunctions is key to addressing parathyroid disorders.