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首页> 外文期刊>Cytokine >Upregulation of neuropilin-1 by basic fibroblast growth factor enhances vascular smooth muscle cell migration in response to VEGF.
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Upregulation of neuropilin-1 by basic fibroblast growth factor enhances vascular smooth muscle cell migration in response to VEGF.

机译：碱性成纤维细胞生长因子上调Neuropilin-1可增强血管平滑肌细胞对VEGF的反应。

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摘要

Neuropilin-1 (NRP-1) is a co-receptor for vascular endothelial growth factor (VEGF). During neovascularization, vascular smooth muscle cells (VSMCs) and pericytes modulate the function of endothelial cells. Factors that mediate NRP-1 in human VSMCs (hVSMCs) remain to be elucidated. We studied various angiogenic cytokines to identify factors that increase NRP-1 expression in hVSMCs. Treatment of hVSMCs with basic fibroblast growth factor (b-FGF) induced expressions of NRP-1 mRNA and protein whereas epidermal growth factor, insulin-like growth factor-1, and interleukin-1beta did not. b-FGF induced phosphorylation of Erk-1/2 and JNK. MEK1/2 and nuclear factor kappa B (NF-kappaB) inhibitors (U0126 and TLCK, respectively) blocked the ability of b-FGF to induce NRP-1 mRNA expression, but inhibition of JNK (SP600125) or PI3-kinase activity (wortmannin) did not. Further, the increase in NRP-1 expression by b-FGF enhanced hVSMCs migration in response to VEGF(165). This effect was dependent on the binding of VEGF(165) to VEGFR-2, as blocking antibodies to VEGFR-2, but not VEGFR-1, inhibited VEGF(165)-induced migration. In conclusion, b-FGF increased NRP-1 expression in hVSMCs that in turn enhance the effect of VEGF(165) on cell migration. The enhanced migration of hVSMCs was mediated through binding of VEGF(165) to both NRP-1 and VEGFR-2, as inhibition of VEGFR-2 on these cells blocked the effect of VEGF-mediated cell migration.
机译：Neuropilin-1（NRP-1）是血管内皮生长因子（VEGF）的共同受体。在新血管形成过程中，血管平滑肌细胞（VSMC）和周细胞调节内皮细胞的功能。在人类VSMC（hVSMC）中介导NRP-1的因素仍有待阐明。我们研究了各种血管生成细胞因子，以鉴定增加hVSMCs中NRP-1表达的因子。用碱性成纤维细胞生长因子（b-FGF）治疗hVSMC诱导NRP-1 mRNA和蛋白表达，而表皮生长因子，胰岛素样生长因子-1和白介素-1β则不表达。 b-FGF诱导Erk-1 / 2和JNK的磷酸化。 MEK1 / 2和核因子kappa B（NF-kappaB）抑制剂（分别为U0126和TLCK）阻断b-FGF诱导NRP-1 mRNA表达的能力，但抑制JNK（SP600125）或PI3激酶活性（渥曼青霉素） ） 没有。此外，b-FGF增加NRP-1的表达增强了hVSMC对VEGF的迁移（165）。这种作用取决于VEGF（165）与VEGFR-2的结合，因为针对VEGFR-2的阻断抗体（而非VEGFR-1）抑制了VEGF（165）诱导的迁移。总之，b-FGF增加了hVSMC中NRP-1的表达，进而增强了VEGF（165）对细胞迁移的作用。 hVSMC迁移的增强是通过VEGF（165）与NRP-1和VEGFR-2的结合而介导的，因为对这些细胞的VEGFR-2抑制作用阻止了VEGF介导的细胞迁移的作用。

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