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Human CC chemokine CCL23, a ligand for CCR1, induces endothelial cell migration and promotes angiogenesis.

机译:人CC趋化因子CCL23(CCR1的配体)诱导内皮细胞迁移并促进血管生成。

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A number of chemokines induce angiogenesis and endothelial cells express several chemokine receptors. To date, only a limited number of CC chemokines for CCR1 have been reported to induce angiogenic responses. We investigated the ability of CCL23 (also known as MPIF-1, MIP-3, or CKbeta8) to promote angiogenesis, which induces chemotaxis of immune cells through CCR1. CCL23 promoted the chemotactic migration and differentiation of endothelial cells, and neovascularization in the chick chorioallantoic membrane. An N-terminal truncated form of CCL23 was at least 100-fold more potent than its intact form and was comparable to that of FGF in the angiogenic activities. Treatment with either pertussis toxin or anti-CCR1 antibody completely inhibited the CCL23-induced endothelial cell migration, indicating that endothelial cell migration was mediated through CCR1. CCL23 didn't promote the migration of HT1080 human fibrosarcoma cells that did not express CCR1. Our results suggest a role of CCL23 in angiogenesis in vitro as well as in vivo.
机译:多种趋化因子诱导血管生成,并且内皮细胞表达几种趋化因子受体。迄今为止,仅报道了有限数量的CCR1 CC趋化因子诱导血管生成反应。我们研究了CCL23(也称为MPIF-1,MIP-3或CKbeta8)促进血管生成的能力,血管生成通过CCR1诱导免疫细胞的趋化性。 CCL23促进了雏鸡绒膜尿囊膜的趋化迁移和内皮细胞分化,以及新血管形成。 CCL23的N末端截短形式的效力比其完整形式至少强100倍,并且在血管生成活性方面与FGF相当。用百日咳毒素或抗CCR1抗体处理可完全抑制CCL23诱导的内皮细胞迁移,表明内皮细胞迁移是通过CCR1介导的。 CCL23不会促进不表达CCR1的HT1080人纤维肉瘤细胞的迁移。我们的结果表明,CCL23在体外和体内均在血管生成中起作用。

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