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首页> 外文期刊>Journal of cellular biochemistry. >VEGF(165) mediates formation of complexes containing VEGFR-2 and neuropilin-1 that enhance VEGF(165)-receptor binding.
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VEGF(165) mediates formation of complexes containing VEGFR-2 and neuropilin-1 that enhance VEGF(165)-receptor binding.

机译：VEGF（165）介导包含VEGFR-2和neuropilin-1的复合物的形成，这些复合物增强了VEGF（165）-受体的结合。

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摘要

Co-expression of NRP1 and (VEGFR-2) KDR on the surface of endothelial cells (EC) enhances VEGF(165) binding to KDR and EC chemotaxis in response to VEGF(165). Overexpression of NRP1 by prostate tumor cells in vivo results in increased tumor angiogenesis and growth. We investigated the molecular mechanisms underlying NRP1-mediated angiogenesis by analyzing the association of NRP1 and KDR. An intracellular complex containing NRP1 and KDR was immunoprecipitated from EC by anti-NRP1 antibodies only in the presence of VEGF(165). In contrast, VEGF(121), which does not bind to NRP1, did not support complex formation. Complexes containing VEGF(165), NRP1, and KDR were also formed in an intercellular fashion by co-culture of EC expressing KDR only, with cells expressing NRP1 only, for example, breast carcinoma cells. VEGF(165) also mediated the binding of a soluble NRP1 dimer to cells expressing KDR only, confirming the formation of such complexes. Furthermore, the formation of complexes containing KDR and NRP1 markedly increased (125)I-VEGF(165) binding to KDR. Our results suggest that formation of a ternary complex of VEGF(165), KDR, and NRP1 potentiates VEGF(165) binding to KDR. These complexes are formed on the surface of EC and in a juxtacrine manner via association of tumor cell NRP1 and EC KDR.
机译：NRP1和（VEGFR-2）KDR在内皮细胞（EC）表面的共表达可增强VEGF（165）与KDR的结合以及EC对VEGF（165）的趋化作用。体内前列腺肿瘤细胞过度表达NRP1会导致肿瘤血管生成和生长增加。我们通过分析NRP1和KDR的关联，调查了NRP1介导的血管生成的分子机制。仅在VEGF存在的情况下，抗NRP1抗体才能从EC中免疫沉淀含有NRP1和KDR的细胞内复合物（165）。相反，不与NRP1结合的VEGF（121）不支持复合物的形成。通过仅将表达KDR的EC与仅表达NRP1的细胞（例如乳腺癌细胞）共培养，还以细胞间的方式形成了含有VEGF（165），NRP1和KDR的复合物。 VEGF（165）还介导了可溶性NRP1二聚体与仅表达KDR的细胞的结合，从而证实了这种复合物的形成。此外，包含KDR和NRP1的复合物的形成显着增加（125）I-VEGF（165）与KDR的结合。我们的结果表明，VEGF（165），KDR和NRP1三元复合物的形成增强了VEGF（165）与KDR的结合。这些复合物通过肿瘤细胞NRP1和EC KDR的缔合在EC的表面上并以并列形式形成。

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