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Related Experiment Videos

Retinoic acid effects on endothelial cell function: interaction with interleukin 1

G Spencer-Green1

  • 1Department of Immunology and Rheumatology, Veteran's Hospital, White River Junction, Vermont 05009.

Clinical Immunology and Immunopathology
|July 1, 1994
PubMed
Summary

Retinoic acid (RA) modifies interleukin-1 (IL-1) effects on endothelial cells, impacting angiogenesis in inflammatory arthritis. This interaction influences cell proliferation, prostacyclin, and PAI-1 production, potentially altering synovitis progression.

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Area of Science:

  • Endocrinology
  • Cell Biology
  • Immunology

Background:

  • Chronic synovitis involves blood vessel angiogenesis, potentially regulated by inflammatory cytokines like interleukin-1 (IL-1).
  • Retinoic acid (RA) is known to influence inflammatory arthritic diseases, possibly by affecting fibroblast collagenase and PGE2 production.

Purpose of the Study:

  • To investigate the interaction between retinoic acid (RA) and interleukin-1 (IL-1) on endothelial cell (EC) function.
  • To determine how RA modifies IL-1's effects on EC proliferation, prostacyclin production, and plasminogen activator inhibitor (PAI-1) capacity.

Main Methods:

  • Cultured endothelial cells (ECs) were treated with varying concentrations of cis- and trans-retinoic acid, retinol, and IL-1.
  • Assessed [3H]TdR uptake for EC proliferation.

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  • Measured prostacyclin production.
  • Quantified plasminogen activator inhibitor capacity (PAI-1) synthesis.

    • Main Results:

    • RA and retinol increased EC proliferation, an effect blocked by IL-1.
    • RA enhanced IL-1-mediated prostacyclin production in ECs, independent of cyclooxygenase (COX).
    • Both IL-1 and RA stimulated EC PAI-1 synthesis, with additive effects observed.

    Conclusions:

    • RA directly affects EC function and modifies IL-1's impact on proliferation, prostacyclin, and PAI-1 production.
    • The interaction between RA and IL-1 on endothelium may influence how RA affects synovitis in experimental inflammatory arthritis.