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开发一种对 Ang2 抑制作用具有正交 Tie2 配体抗性的配体。

Development of an Orthogonal Tie2 Ligand Resistant to Inhibition by Ang2.

机构信息

Department of Cardiovascular Sciences and Department of Molecular and Cell Biology , University of Leicester , Henry Wellcome Building, Lancaster Road , Leicester LE1 7RH , U.K.

出版信息

Mol Pharm. 2018 Sep 4;15(9):3962-3968. doi: 10.1021/acs.molpharmaceut.8b00409. Epub 2018 Aug 6.

Abstract

Angiopoietin-1 (Ang1) is a vascular protective ligand that acts through the receptor tyrosine kinase Tie2 to enhance endothelial survival and quiescence. In sepsis, diabetic retinopathy, and a range of other diseases, Ang2, an antagonist of Tie2, increases markedly. This antagonist suppresses Ang1 protective effects leading to vascular destabilization, inflammation, and endothelial death. Administration of recombinant Ang1 can counter Ang2 antagonism and restore vascular function. However, recombinant Ang1 is needed at sufficiently high concentrations to block Ang2, and the protein is difficult to produce, requires mammalian expression systems, and is prone to aggregation. Here we present an engineered synthetic Tie2 ligand that is not antagonized by Ang2 but is easy to produce and more robust than Ang1. Using a peptide phage display, we isolated a heptameric sequence that binds Tie2-ectodomain and fused this to the coiled:coil domain of cartilage oligomeric matrix protein. This pentameric protein is 60 kDa in size, expressed in E. coli, and facile to purify. The protein, designated TSL1, binds to Tie2-ectodomain in vitro and on the cell surface. TSL1 inhibits endothelial apoptosis. Crucially, TSL1 binds at a site on Tie2 distinct from the angiopoietin-binding site and is resistant to antagonism by Ang2. This engineered ligand has several advantages over recombinant Ang1 for potential therapeutic applications. The study also highlights the value of orthogonal ligands for regulating cellular receptors without being subject to antagonism or modulation by endogenous ligands.

摘要

血管生成素-1(Ang1)是一种血管保护配体,通过受体酪氨酸激酶 Tie2 发挥作用,增强内皮细胞的存活和静止。在败血症、糖尿病性视网膜病变和一系列其他疾病中,Tie2 的拮抗剂 Ang2 显著增加。这种拮抗剂抑制 Ang1 的保护作用,导致血管不稳定、炎症和内皮细胞死亡。给予重组 Ang1 可以对抗 Ang2 的拮抗作用并恢复血管功能。然而,重组 Ang1 需要足够高的浓度来阻断 Ang2,而且该蛋白难以生产,需要哺乳动物表达系统,并且容易聚集。在这里,我们提出了一种工程合成的 Tie2 配体,它不会被 Ang2 拮抗,但易于生产,比 Ang1 更稳健。我们使用肽噬菌体展示技术分离出一种与 Tie2-胞外结构域结合的七聚体序列,并将其融合到软骨寡聚基质蛋白的卷曲:卷曲结构域。这种五聚体蛋白大小为 60 kDa,在大肠杆菌中表达,易于纯化。该蛋白命名为 TSL1,在体外和细胞表面与 Tie2-胞外结构域结合。TSL1 抑制内皮细胞凋亡。至关重要的是,TSL1 结合 Tie2 的位点与血管生成素结合位点不同,并且不易受 Ang2 的拮抗作用影响。与重组 Ang1 相比,这种工程化配体具有治疗应用的几个优势。该研究还强调了正交配体在调节细胞受体而不受内源性配体拮抗或调节的价值。

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