Shi R J, Simpson-Haidaris P J, Marder V J, Silverman D J, Sporn L A
Department of Medicine, University of Rochester School of Medicine and Dentistry, New York, USA.
Thromb Haemost. 1996 Apr;75(4):600-6.
Changes in PAI-1 expression in human umbilical vein endothelial cells (HUVEC) were studied following in vitro infection with Rickettsia rickettsii. A 1.8-fold increase in secreted PAI-1 activity occurred in infected versus control cultures (p = 0.03) at 24 h but not at earlier timepoints. A similar increase (1.4-fold) in secreted PAI-1 antigen (p < 0.005) was measured by ELISA. To determine whether this increase was due to increased synthesis of PAI-1, HUVEC were metabolically labeled with 35S-methionine concurrent with R. rickettsii infection. Such infection resulted in a 1.9-fold increase in labeled PAI-1 in the medium at 24 h (p = 0.036). Increase steady-state levels of PAI-1 mRNA were detected as early as 18 h by Northern blot analysis, peaking (5.5-fold) at approximately 24 h. These results indicate that PAI-1 production is increased in RR-infected endothelial cells, an effect that may contribute to the vascular occlusions noted in Rocky Mountain spotted fever.
在用立氏立克次体进行体外感染后,研究了人脐静脉内皮细胞(HUVEC)中纤溶酶原激活物抑制剂-1(PAI-1)表达的变化。在感染24小时时,与对照培养物相比,感染培养物中分泌的PAI-1活性增加了1.8倍(p = 0.03),但在更早的时间点未出现这种情况。通过酶联免疫吸附测定法(ELISA)检测到分泌的PAI-1抗原也有类似的增加(1.4倍)(p < 0.005)。为了确定这种增加是否是由于PAI-1合成增加所致,在用立氏立克次体感染的同时,用人脐静脉内皮细胞进行35S-甲硫氨酸代谢标记。这种感染导致24小时时培养基中标记的PAI-1增加了1.9倍(p = 0.036)。通过Northern印迹分析,早在18小时就检测到PAI-1 mRNA的稳态水平增加,在大约24小时达到峰值(5.5倍)。这些结果表明,在感染立氏立克次体的内皮细胞中PAI-1的产生增加,这种效应可能导致落基山斑疹热中出现的血管闭塞。