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Related Experiment Videos

Identifying and characterizing the joint cavity-forming cell.

Andrew A Pitsillides1

  • 1Department of Veterinary Basic Sciences, Royal Veterinary College, London, UK. apitsill@rvc.ac.uk

Cell Biochemistry and Function
|August 12, 2003
PubMed
Summary
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Mechanical stimuli, like skeletal movement, promote joint development by influencing fibroblast-like cells. This process involves the activation of mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) signaling pathways.

Area of Science:

  • Biochemistry
  • Developmental Biology
  • Cell Biology

Background:

  • Synovial fluid hyaluronan production was long attributed to the synovial membrane.
  • Fibroblast-like cells on the synovial lining contribute to glycosaminoglycan levels.
  • Mechanisms controlling differentiated cell phenotypes in joint development were unclear.

Purpose of the Study:

  • Investigate mechanisms controlling differentiated cell phenotypes during embryonic joint development.
  • Identify upstream mechano-dependent factors controlling these events.
  • Elucidate the role of MAPK/ERK signaling in joint cavitation and cell differentiation.

Main Methods:

  • Quantitative cytochemical techniques for uridine-diphospho glucose dehydrogenase (UDPGD) activity.
  • In situ micro-biochemical studies on embryonic limb development.

Related Experiment Videos

  • Immunolabelling using phospho-specific anti-ERK-1/2 antibodies.
  • In vitro studies using Western blotting and mechanical strain on cultured cells.
  • Pharmacological inhibition of ERK activation using PD98059.

    • Main Results:

    • Cells bordering presumptive joint cavities show increased UDPGD activity and hyaluronan-rich matrix.
    • Immobilization leads to loss of these characteristics, suggesting mechanical stimuli promote joint line formation.
    • Joint line-selective activation of ERK-1/2 occurs during embryonic limb cavitation, abolished by immobilization.
    • Mechanical strain increases active ERK-1/2 expression in cultured articular cells.
    • Inhibition of ERK activation enhances strain-induced UDPGD mRNA expression, indicating a feedback role.

    Conclusions:

    • Mechanical stimuli are crucial for acquiring the joint line-forming phenotype during embryonic development.
    • MAPK/ERK signaling is involved in mechano-transduction during joint cavitation.
    • ERK activation appears to have a feedback regulatory role in the differentiation of articular surface cells.
    • Bridging in vitro findings with in vivo cell-cell and cell-matrix interactions is essential for a complete understanding.