...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Prevention of experimental antiphospholipid syndrome and endothelial cell activation by snthetic peptides
【24h】

Prevention of experimental antiphospholipid syndrome and endothelial cell activation by snthetic peptides

机译：合成肽预防实验性抗磷脂综合征和内皮细胞活化

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Antiphospholipid syndrome (APS) is char- acterized by recurrent fetal loss, repeated thromboembolic phenomena, and thrombocytopenia. The syndrome is believed to be caused by antiphospholipid beta-2-glycoprotein-I (#beta#2GPI)-dependent Abs or anti-#beta#2GPI Abs by themselves. Using a hexapeptide phage display library, we identified three hexapeptides that react specifically with the anti-#beta#2GPI mAbs ILA-1, ILA-3, and H-3, which cause endothelial cell activation and induce experimental APS. To enhance the binding of the peptides to the corresponding mAbs, the peptides were length- ened to correspond with the site of the #beta#2GPI epitope being recognized by these mAbs. As a result, the following three peptides were prepared: A, NTLKTPRVGGC, which binds to ILA-1 mAb; B, KDKATFGCHDGC, which binds to ILA-3 mAb; and C, CATLRVYKGG, which binds to H-3 mAb. Peptides A, B, and C specifically inhibit both in vitro and in vivo the biological functions of the corresponding anti-#beta#2GPI mAbs. Exposure of endothelial cells to anti-#beta#2GPI mAbs and their corresponding peptides led to the inhibition of endothe- lial cell activation, as shown by decreased expression of adhesion molecules (E-selectin, ICAM-1, VCAM-1) and mono- cyte adhesion. In vivo infusion of each of the anti-#beta#2GPI mAbs into BALB/c mice, followed by administration of the corre- sponding specific peptides, prevented the peptide-treated mice from developing experimental APS. The use of synthetic peptides that focus on neutralization of pathogenic anti- #beta#2GPI Abs represents a possible new therapeutic app
机译：抗磷脂综合症（APS）的特征是胎儿反复发作，反复出现血栓栓塞现象和血小板减少症。该综合征被认为是由抗磷脂β-2-糖蛋白-I（＃beta＃2GPI）依赖性抗体或抗＃β＃2GPI Abs抗体本身引起的。使用六肽噬菌体展示文库，我们鉴定了三种与抗＃beta＃2GPI mAb ILA-1，ILA-3和H-3特异性反应的六肽，这会引起内皮细胞激活并诱导实验性APS。为了增强肽与相应mAb的结合，将肽加长以对应于被这些mAb识别的＃beta＃2GPI表位的位点。结果，制备了以下三种肽：A，与ILA-1 mAb结合的NTLKTPRVGGC；和B，KDKATFGCHDGC，其结合ILA-3 mAb； C为CATLRVYKGG，与H-3 mAb结合。肽A，B和C在体内和体外均特异性抑制相应的抗＃β＃2GPI mAb的生物学功能。内皮细胞暴露于抗＃β＃2GPI mAb及其相应的肽导致内皮细胞激活受到抑制，如粘附分子（E-选择素，ICAM-1，VCAM-1）和单核糖核酸的表达降低所表明的-细胞粘附。将每种抗＃β＃2GPI mAb体内注入BALB / c小鼠后，再施用相应的特定肽，可防止用肽处理的小鼠产生实验性APS。专注于中和病原性抗＃β＃2GPI Abs的合成肽的使用代表了一种可能的新治疗应用

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号