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

GM-CSF cannot substitute for M-CSF in human osteoclastogenesis.

Jason M Hodge1, Mark A Kirkland, Geoffrey C Nicholson

  • 1Department of Clinical and Biomedical Sciences, Barwon Health, University of Melbourne, Geelong, Victoria 3220, Australia. j.hodgel@pgrad.unimelb.edu.au

Biochemical and Biophysical Research Communications
|September 11, 2004
PubMed
Summary

Granulocyte-macrophage colony-stimulating factor (GM-CSF) enhances human osteoclastogenesis, but this effect is dependent on macrophage colony-stimulating factor (M-CSF). GM-CSF does not directly replace M-CSF in this process.

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

Psychotropic medication use and bone loss in men: longitudinal study.

BJPsych open·2026
Same author

The neglected association between schizophrenia and bone fragility: a systematic review and meta-analyses.

Translational psychiatry·2024
Same author

Lithium use and bone health in women with bipolar disorder: A cross-sectional study.

Acta psychiatrica Scandinavica·2024
Same author

Randomised trial of genetic testing and targeted intervention to prevent the development and progression of Paget's disease of bone.

Annals of the rheumatic diseases·2023
Same author

Biofabrication of functional bone tissue: defining tissue-engineered scaffolds from nature.

Frontiers in bioengineering and biotechnology·2023
Same author

Antipsychotic medication use and fracture: a case-control study.

Scientific reports·2023

Area of Science:

  • Cell Biology
  • Immunology
  • Hematopoiesis

Background:

  • Osteopetrosis is a bone disorder characterized by impaired osteoclast function.
  • Mice lacking M-CSF show age-related recovery from osteopetrosis, suggesting alternative pathways for osteoclast formation.
  • GM-CSF has been investigated as a potential therapeutic agent for osteoclast disorders.

Purpose of the Study:

  • To investigate if GM-CSF can substitute for M-CSF in human osteoclastogenesis in vitro.
  • To elucidate the role of GM-CSF in human osteoclast differentiation.

Main Methods:

  • Human CFU-GM precursors were cultured with RANKL to induce osteoclast differentiation.
  • M-CSF dependence was assessed using M-CSF antibodies.
  • The effects of varying GM-CSF concentrations and durations were evaluated.

Related Experiment Videos

  • M-CSF mRNA expression was analyzed following GM-CSF treatment.
  • FLT3-ligand and VEGF were tested for their ability to support osteoclastogenesis.

    • Main Results:

    • Human osteoclastogenesis occurred constitutively in the presence of RANKL, indicating endogenous M-CSF production.
    • M-CSF antibody completely inhibited osteoclast differentiation, confirming M-CSF dependence.
    • GM-CSF enhanced osteoclastogenesis at specific concentrations and durations, but this effect was abrogated by M-CSF antibody.
    • GM-CSF transiently increased M-CSF mRNA but suppressed it long-term.
    • FLT3-ligand and VEGF did not support osteoclastogenesis without M-CSF.

    Conclusions:

    • In vitro human osteoclastogenesis is critically dependent on M-CSF.
    • The osteoclastogenic effects of GM-CSF are mediated through M-CSF.
    • GM-CSF is unlikely to rescue M-CSF deficiency directly via FLT3-ligand or VEGF pathways.