Reininger A J, Korndörfer M A, Wurzinger L J
Anatomisches Institut, Technische Universität München, Germany.
Thromb Haemost. 1998 May;79(5):998-1003.
As we demonstrated earlier, platelets adhere to intact endothelium provided they are activated and convectively transported against the endothelial surface. To identify the platelet receptors involved we superfused cultured endothelium with activated platelet rich plasma (PRP) by means of the Stagnation Point Flow Adhesio- Aggregometer while blocking various platelet receptors. Inhibition was performed with the tetrapeptide RGDS, the non-peptide Ro-43-8857, or a monoclonal antibody directed against integrin alphaIIbeta3. Platelet deposition was video-recorded and quantified by image analysis. Infusion of RGDS or Ro-43-8857 into ADP-stimulated PRP completely prevented adhesion as well as subsequent aggregation. Interrupting the inhibitor infusion while ADP stimulation persisted, prompted adhesion and aggregation, demonstrating the reversibility of the inhibition. Platelet adhesion was irreversibly blocked by preincubation of the PRP with the moab against alphaIIbeta3. Its specific binding was confirmed by immunoelectron microscopy. Our results suggest that platelet adhesion to intact endothelium is mediated via platelet integrin alphaIIbeta3.
正如我们之前所证明的，血小板只要被激活并逆着内皮表面进行对流运输，就会黏附于完整的内皮。为了确定所涉及的血小板受体，我们通过驻点流黏附聚集仪，用激活的富含血小板血浆（PRP）灌注培养的内皮，同时阻断各种血小板受体。使用四肽RGDS、非肽Ro-43-8857或针对整合素αIIβ3的单克隆抗体进行抑制。通过图像分析对血小板沉积进行视频记录和定量。将RGDS或Ro-43-8857注入ADP刺激的PRP中，可完全阻止黏附以及随后的聚集。在ADP刺激持续的情况下中断抑制剂注入，会促使黏附和聚集，表明抑制作用是可逆的。用针对αIIβ3的单克隆抗体对PRP进行预孵育，可不可逆地阻断血小板黏附。免疫电子显微镜证实了其特异性结合。我们的结果表明，血小板与完整内皮的黏附是通过血小板整合素αIIβ3介导的。
