Berliner J A, Territo M, Almada L, Carter A, Shafonsky E, Fogelman A M
Arteriosclerosis. 1986 May-Jun;6(3):254-8. doi: 10.1161/01.atv.6.3.254.
Cultured rabbit aortic and human carotid artery endothelial cells produced a factor that was chemotactic for monocytes but not for neutrophils. Checkerboard analysis showed that the activity was due to chemotaxis and not to chemokinesis. The factor was produced in both serum-containing and serumless media. Treatment with carboxypeptidase and trypsin resulted in inhibition of chemotactic activity, indicating that the factor is a peptide. Medium from cultures of rabbit aortic, human carotid artery, and human umbilical vein endothelial cells previously exposed to beta migrating very low density lipoprotein (beta-VLDL) had substantially more chemotactic activity than medium from untreated cells or cells exposed to low density lipoprotein. beta-VLDL alone had no chemotactic activity. We conclude that large vessel endothelial cells produce a monocyte chemotactic factor that is increased after exposure of the cells to beta-VLDL.
培养的兔主动脉内皮细胞和人颈动脉内皮细胞产生一种对单核细胞具有趋化作用但对中性粒细胞无趋化作用的因子。棋盘分析表明，该活性是由于趋化作用而非趋化运动。该因子在含血清和无血清培养基中均能产生。用羧肽酶和胰蛋白酶处理会导致趋化活性受到抑制，这表明该因子是一种肽。先前暴露于β迁移极低密度脂蛋白（β-VLDL）的兔主动脉、人颈动脉和人脐静脉内皮细胞培养物的培养基，其趋化活性明显高于未处理细胞或暴露于低密度脂蛋白的细胞的培养基。单独的β-VLDL没有趋化活性。我们得出结论，大血管内皮细胞产生一种单核细胞趋化因子，细胞暴露于β-VLDL后该因子会增加。
