Hamilton J H, Bootes A, Phillips P E, Slywka J
Arthritis Rheum. 1981 Oct;24(10):1296-303. doi: 10.1002/art.1780241010.
Human synovial fibroblasts in culture have been shown to have low plasminogen activator (PA) activity; however, conditioned medium from concanavalin A-stimulated peripheral blood mononuclear cells (c-MCCM) stimulates the cellular levels of this protease. The present study shows that low concentrations of a series of antiinflammatory steroids inhibit the PA activities of both unstimulated and c-MCCM-stimulated fibroblasts. Dexamethasone, the corticosteroid studied in greatest detail, suppresses both the extracellular and cell-associated enzyme activities; this inhibition is rapid, reversible, and is not due to the inhibition of cellular RNA, protein, or DNA synthesis. PA has been invoked as possibly being generally important for the processes of cell migration, tissue remodeling, and inflammation. These in vitro observations suggest that physiologic and/or pharmacologic control of the PA levels in synovial fibroblasts might also be achieved in vivo by the interacting effects of mutually antagonistic agents, namely, a product from stimulated mononuclear cells and glucocorticoids.
培养的人滑膜成纤维细胞已被证明具有较低的纤溶酶原激活物（PA）活性；然而，伴刀豆球蛋白A刺激的外周血单核细胞的条件培养基（c-MCCM）可刺激这种蛋白酶的细胞水平。本研究表明，低浓度的一系列抗炎类固醇可抑制未刺激和c-MCCM刺激的成纤维细胞的PA活性。地塞米松是研究最为详细的皮质类固醇，它可抑制细胞外和细胞相关的酶活性；这种抑制作用迅速、可逆，且不是由于细胞RNA、蛋白质或DNA合成受到抑制。PA被认为可能在细胞迁移、组织重塑和炎症过程中普遍具有重要作用。这些体外观察结果表明，滑膜成纤维细胞中PA水平的生理和/或药理控制在体内也可能通过相互拮抗的物质（即刺激的单核细胞产物和糖皮质激素）的相互作用来实现。
