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血小板活化因子体外诱导血小板与白细胞相互作用黏附于内皮细胞的研究

Platelet-leukocyte interaction in adhesion to endothelial cells induced by platelet-activating factor in vitro.

作者信息

Hirafuji M, Shinoda H

机构信息

Department of Pharmacology, Tohoku University School of Dentistry, Sendai, Japan.

出版信息

Br J Pharmacol. 1991 Jun;103(2):1333-8. doi: 10.1111/j.1476-5381.1991.tb09789.x.

Abstract
  1. Platelet-activating factor (PAF, 10 nM) did not induce platelet adhesion to endothelial cells cultured in monolayer but it induced their adhesion to protein-coated plastic. However, PAF induced a marked platelet adhesion to endothelial cells when polymorphonuclear leukocytes (PMNs) were present. Lyso-PAF had no effect. 2. Phase-contrast microscopic examination showed that single platelets rather than their aggregates adhered to the endothelial cell surface around aggregating and adhering PMNs. 3. Significant platelet adhesion was induced by PAF at concentrations higher that 0.01 nM with the maximal response at 10 nM. Platelet adhesion occurred within minutes after PAF addition, reaching a maximum approximately after 30 min. Platelet adhesion also occurred significantly at a PMN:platelet ratio of 1:800, and linearly up to 1:50. 4. The PAF-induced platelet adhesion was suppressed by three structurally unrelated PAF antagonists, WEB 2086, ONO 6240 and BN 52021, in a concentration-dependent manner. 5. PAF also increased PMN adhesion to endothelial cell monolayers, which was further augmented by the presence of platelets. 6. The present study demonstrates that PAF induces platelet adhesion to endothelial cells in vitro when PMNs are present and that there is a close interaction between platelets and PMNs in their adhesion to endothelial cells. The present study further suggests that PMNs could play a central role in platelet adhesion to vascular endothlium in certain pathological conditions.
摘要
  1. 血小板活化因子(PAF,10 nM)不会诱导血小板黏附于单层培养的内皮细胞,但会诱导其黏附于蛋白包被的塑料表面。然而,当存在多形核白细胞(PMN)时,PAF会诱导血小板显著黏附于内皮细胞。溶血PAF没有作用。2. 相差显微镜检查显示,单个血小板而非其聚集体黏附于聚集和黏附的PMN周围的内皮细胞表面。3. 浓度高于0.01 nM的PAF可诱导显著的血小板黏附,最大反应浓度为10 nM。PAF添加后数分钟内发生血小板黏附,约30分钟后达到最大值。PMN与血小板比例为1:800时也会显著发生血小板黏附,直至1:50时呈线性增加。4. 三种结构不相关的PAF拮抗剂WEB 2086、ONO 6240和BN 52021以浓度依赖性方式抑制PAF诱导的血小板黏附。5. PAF还增加了PMN对内皮细胞单层的黏附,血小板的存在进一步增强了这种黏附。6. 本研究表明,当存在PMN时,PAF在体外诱导血小板黏附于内皮细胞,并且血小板与PMN在黏附于内皮细胞方面存在密切相互作用。本研究进一步表明,在某些病理条件下,PMN可能在血小板黏附于血管内皮中起核心作用。
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c35/1908373/3d2d7e94c88d/brjpharm00236-0059-a.jpg

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