Platelet‐derived growth factor potentiates cellular responses of articular chondrocytes to interleukin‐1

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Abstract
Recombinant human interleukin‐1α (IL‐1α) induced a time‐dependent (0–72 hours) and concentration‐dependent (0.01–10 ng/ml) production of metalloproteinases (collagenase, gelatinase, stromelysin) and prostaglandin E2 (PGE2) in rabbit articular chondrocytes (RAC). Exposure of RAC to recombinant human platelet‐derived growth factor homodimer BB (PDGF‐BB; 2–200 ng/ml) in the presence of stimulatory and substimulatory concentrations of IL‐1α resulted in a marked augmentation of metalloproteinase and PGE2 production. PDGF‐BB exerted no agonist effects on RAC responsiveness. PDGF‐BB up‐regulated the number of IL‐1 receptors per chondrocyte but had no effect on receptor affinity. Cycloheximide and actinomycin D caused a concentration‐dependent suppression of the PDGF‐BB–mediated potentiation of radiolabeled IL‐1α binding to RAC and cell responsiveness to IL‐1α. Similarly, IL‐1 increased the number of PDGF receptors on RAC without changing receptor affinity. These data are discussed within the context of cytokine–growth factor interactions as components of the pathogenesis of arthritic diseases.