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首页> 外文期刊>Journal of Cell Science >The soluble D2D3(88-274) fragment of the urokinase receptor inhibits monocyte chemotaxis and integrin-dependent cell adhesion
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The soluble D2D3(88-274) fragment of the urokinase receptor inhibits monocyte chemotaxis and integrin-dependent cell adhesion

机译：尿激酶受体的可溶性D2D3（88-274）片段抑制单核细胞趋化性和整合素依赖性细胞粘附

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We have previously shown that chymotrypsin-cleaved soluble uPAR (D2D3(88-274)) elicits migration of monocytic cells through interaction with FPRL-1, a G protein-coupled receptor that is homologous to the fMLP receptor. Here, we report that D2D3(88-274) also modulates the ability of monocytes to migrate in response to other chemokines. Pretreatment of monocytes with increasing amounts of D2D3(88-274) prevents cell migration in response to MCP-1, RANTES and fMLP. We demonstrate that D2D3(388-274) does not inhibit MCP-1 receptor binding, elicit CCR2 internalization and prevent MCP-1-induced intracellular Ca2+ increase. Thus, CCR2 receptor desensitization cannot account for D2D3(88-274-)mediated inhibition of MCP-1-induced cell. migration. Rather, we show that pretreatment of monocytes with D2D3(88-274) dramatically decreases chemokine-induced integrin-dependent rapid cell adhesion by interacting with FPRL-1. Together our results indicate that chemokine-dependent cell migration can be regulated not only by homologous and heterologous receptor desensitization, but also by inhibition of integrin-dependent cell adhesion, an important step. in cell transmigration.
机译：以前我们已经表明，胰凝乳蛋白酶切割的可溶性uPAR（D2D3（88-274））通过与FPRL-1（与fMLP受体同源的G蛋白偶联受体）相互作用引发单核细胞迁移。在这里，我们报告D2D3（88-274）还调节响应于其他趋化因子单核细胞迁移的能力。用增加量的D2D3（88-274）预处理单核细胞可防止细胞响应MCP-1，RANTES和fMLP迁移。我们证明，D2D3（388-274）不抑制MCP-1受体结合，引起CCR2内化并防止MCP-1诱导的细胞内Ca2 +增加。因此，CCR2受体脱敏不能解释D2D3（88-274-）介导的MCP-1诱导的细胞抑制。移民。而是，我们显示，通过与FPRL-1相互作用，用D2D3（88-274）对单核细胞进行预处理可显着降低趋化因子诱导的整合素依赖性快速细胞粘附。我们的研究结果共同表明，趋化因子依赖性细胞迁移不仅可以通过同源和异源受体脱敏来调节，而且可以通过抑制整联蛋白依赖性细胞粘附这一重要步骤来调节。在细胞迁移中。

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