Related Experiment Videos
Retinoic acid effects on endothelial cell function: interaction with interleukin 1
1Department of Immunology and Rheumatology, Veteran's Hospital, White River Junction, Vermont 05009.
Clinical Immunology and Immunopathology
|July 1, 1994
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.
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.
- 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.