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Related Concept Videos

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The gastric mucosa produces prostaglandins E2 (PGE2) and prostacyclin (PGI2), crucial in maintaining gastric health. They exert cytoprotective effects, including increasing bicarbonate secretion, releasing protective mucin, reducing gastric acid output, and preventing harmful vasoconstriction. These effects are mediated through various receptors, such as EP1, EP2, EP3, and EP4.
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Related Experiment Video

Updated: Jun 17, 2026

A Novel in vivo Gene Transfer Technique and in vitro Cell Based Assays for the Study of Bone Loss in Musculoskeletal Disorders
11:47

A Novel in vivo Gene Transfer Technique and in vitro Cell Based Assays for the Study of Bone Loss in Musculoskeletal Disorders

Published on: June 8, 2014

Prostaglandins in bone: bad cop, good cop?

Katherine A Blackwell1, Lawrence G Raisz, Carol C Pilbeam

  • 1New England Musculoskeletal Institute, University of Connecticut Health Center, 263 Farmington Ave, Farmington, CT, USA.

Trends in Endocrinology and Metabolism: TEM
|January 19, 2010
PubMed
Summary

Prostaglandins (PGs) regulate bone metabolism, influencing both resorption and formation. Understanding their signaling pathways, particularly involving cyclooxygenase-2 (COX-2), is key to skeletal health and disease.

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Last Updated: Jun 17, 2026

A Novel in vivo Gene Transfer Technique and in vitro Cell Based Assays for the Study of Bone Loss in Musculoskeletal Disorders
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07:00

Intra-iliac Artery Injection for Efficient and Selective Modeling of Microscopic Bone Metastasis

Published on: September 26, 2016

Area of Science:

  • Bone Biology
  • Molecular Signaling
  • Skeletal Physiology

Background:

  • Prostaglandins (PGs) are key regulators of bone metabolism.
  • They influence both bone resorption and formation processes.
  • PGs are implicated in inflammatory bone loss, metastatic bone disease, fracture healing, and heterotopic ossification.

Purpose of the Study:

  • To explore the role of inducible cyclooxygenase (COX)-2 and prostaglandin E2 (PGE2) receptors in bone metabolism.
  • To investigate the extensive G-protein signaling network engaged by PGs.
  • To elucidate the regulation of skeletal cell growth in health and disease.

Main Methods:

  • Analysis of cyclooxygenase-2 (COX)-2 expression and activity.
  • Investigation of prostaglandin E2 (PGE2) receptor signaling pathways.
  • Examination of downstream G-protein signaling in skeletal cells.

Main Results:

  • Recent studies highlight the involvement of COX-2 and PGE2 receptors in bone remodeling.
  • PGs activate not only cAMP/PKA pathways but also broader G-protein signaling networks.
  • These pathways are crucial in processes like fracture healing and inflammatory bone resorption.

Conclusions:

  • Further research into COX-2 and PG receptors is essential for understanding bone regulation.
  • Targeting these G-protein signaling pathways could offer therapeutic strategies for bone diseases.
  • Elucidating these mechanisms provides insights into skeletal cell growth in both physiological and pathological conditions.