Hamilton J A, Wojta J, Gallichio M, McGrath K, Filonzi E L
University of Melbourne, Department of Medicine, Royal Melbourne Hospital, Parkville, Australia.
J Immunol. 1993 Nov 15;151(10):5154-61.
TGF-beta increased in a dose-dependent manner the production of plasminogen activator inhibitor-1 (PAI-1) in cultured human synovial fibroblast-like cells, as measured by ELISA. Significant increases in PAI-1 were first detected in cell supernatants within 4 h after cytokine addition. Increases were also observed in PAI-1 mRNA expression. IL-1 suppressed these increases in PAI-1 Ag and mRNA. In contrast, when PAI-2 levels were measured by ELISA, TGF-beta did not raise them but inhibited slightly the enhancement caused by IL-1 of PAI-2 Ag and mRNA. Therefore TGF-beta selectively stimulates the formation of one PAI; TGF-beta and IL-1 have opposing effects on PAI-1 and PAI-2 synthesis in the synovial cells. These findings are proposed to help define the control of fibrinolysis and tissue remodeling in the rheumatoid synovium.
通过酶联免疫吸附测定法（ELISA）检测发现，转化生长因子-β（TGF-β）以剂量依赖方式增加培养的人滑膜成纤维样细胞中纤溶酶原激活物抑制剂-1（PAI-1）的产生。细胞因子添加后4小时内，首先在细胞上清液中检测到PAI-1显著增加。PAI-1 mRNA表达也有增加。白细胞介素-1（IL-1）抑制了PAI-1抗原和mRNA的这些增加。相反，当通过ELISA测量PAI-2水平时，TGF-β并未使其升高，而是略微抑制了IL-1引起的PAI-2抗原和mRNA的增强。因此，TGF-β选择性地刺激一种PAI的形成；TGF-β和IL-1对滑膜细胞中PAI-1和PAI-2的合成具有相反的作用。这些发现有助于明确类风湿性滑膜中纤维蛋白溶解和组织重塑的调控机制。
