Matsuda T, Takemoto Y, Kishimoto T, Maekawa M, Akutsu T
Dept. of Bioengineering, National Cardiovascular Center, Osaka, Japan.
Biomater Artif Cells Artif Organs. 1990;18(5):579-84. doi: 10.3109/10731199009117324.
The platelet adhesion on adhesive protein-coated surfaces was significantly reduced by the addition of the synthetic tetrapeptide, RGDS (Arg-Gly-Asp-Ser), which was identified as the common amino acid sequence of adhesive site of adhesive proteins. The inhibitory effect was also observed for leukocyte(WBC) in complement-inactivated serum. No significant effect was observed for WBC in complement-activated serum. These indicate that the RGDS ligand-receptor mechanism operates on adhesive protein-adsorbed surfaces for both cellular systems and that activated complement factor (C3b)-membrane receptor (CR3) interaction operates for WBC as the complement is activated.
添加合成四肽RGDS（精氨酸-甘氨酸-天冬氨酸-丝氨酸）后，血小板在粘附蛋白包被表面的粘附显著减少，该四肽被确定为粘附蛋白粘附位点的共同氨基酸序列。在补体失活血清中，白细胞（WBC）也观察到了抑制作用。在补体激活血清中，未观察到白细胞有显著影响。这些表明，RGDS配体-受体机制在细胞系统的粘附蛋白吸附表面均起作用，并且随着补体的激活，活化的补体因子（C3b）-膜受体（CR3）相互作用对白细胞起作用。
