Human CC chemokine CCL23, a ligand for CCR1, induces endothelial cell migration and promotes angiogenesis
Human CC chemokine CCL23, a ligand for CCR1, induces endothelial cell migration and promotes angiogenesis
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DOI：
10.1016/j.cyto.2005.01.018
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发表时间：
2005-06-07
期刊：
影响因子：
3.8
通讯作者：
Kim, J
中科院分区：
文献类型：
--
作者：
Hwang, J;Son, KN;Kim, J
许多趋化因子诱导血管生成，内皮细胞表达多种趋化因子受体。到目前为止，只有数量有限的CCR1趋化因子被报道能诱导血管生成反应。我们研究了CCL23(也称为MPIF-1、MIP-3或CKβ8)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。CCL23可促进鸡胚绒毛尿囊膜内皮细胞的趋化迁移和分化，促进新生血管形成。N端截短形式的CCL23的血管生成活性至少是其完整形式的100倍，与成纤维细胞生长因子相当。百日咳毒素或抗CCR1抗体均可完全抑制CCL23诱导的内皮细胞迁移，提示内皮细胞迁移是通过CCR1介导的。CCL23不能促进不表达CCRL的HT1080人纤维肉瘤细胞的迁移。我们的结果表明，CCL23在体内和体外都有促进血管生成的作用。(C)2005爱思唯尔有限公司。保留所有权利。
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 CK beta 8) 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 CCRL Our results suggest a role of CCL23 in angiogenesis in vitro as well as in vivo. (c) 2005 Elsevier Ltd. All rights reserved.