Carson C W, Hunder G G, Kaplan K L, Johnson C M
Division of Rheumatology, Mayo Clinic/Foundation, Rochester, Minnesota 55905.
Am J Pathol. 1991 Jul;139(1):199-206.
The authors investigated the release of an endothelial cell-specific protein (E92) by cultured porcine aortic endothelial cell cultures. Under normal culture conditions, endothelial cells released little or no E92 into the culture supernatant. Treatment with thrombin (0.01 to 10 units/ml), endotoxin (0.01 to 10 micrograms/ml), or interleukin-1 (0.01 to 3.0 units/ml), however, caused significant, dose-dependent increases in E92 detectable in the culture supernatants. Time-course experiments showed that maximum release of E92 into cellular supernatants occurred 24 hours after stimulation with all mediators. Parallel experiments used 51Cr-loaded endothelial cells as a measure of lethal cellular injury. None of the mediators caused significant injury at the doses observed to induce release of E92. These results suggest that the release of E92 into the supernatants of cultured endothelial cells is an inducible event. The data also support the hypothesis that detection of E92 antigen in sera from patients with rheumatic disease represents a marker of in vivo vascular endothelial cell activity.
作者研究了培养的猪主动脉内皮细胞培养物中一种内皮细胞特异性蛋白(E92)的释放情况。在正常培养条件下,内皮细胞向培养上清液中释放很少或不释放E92。然而,用凝血酶(0.01至10单位/毫升)、内毒素(0.01至10微克/毫升)或白细胞介素-1(0.01至3.0单位/毫升)处理后,培养上清液中可检测到的E92显著增加,且呈剂量依赖性。时间进程实验表明,在用所有介质刺激后24小时,E92释放到细胞上清液中的量达到最大值。平行实验使用51Cr标记的内皮细胞作为致死性细胞损伤的指标。在观察到诱导E92释放的剂量下,没有一种介质会造成显著损伤。这些结果表明,E92释放到培养的内皮细胞上清液中是一个可诱导的事件。数据还支持这样的假设,即检测风湿性疾病患者血清中的E92抗原代表体内血管内皮细胞活性的一个标志物。