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Cornin induces angiogenesis through PI3K-Akt-eNOS-VEGF signaling pathway

机译:Cornin通过PI3K-Akt-eNOS-VEGF信号通路诱导血管生成

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摘要

In the present study, we sought to elucidate whether Cornin contributes to induce angiogenesis and its mechanisms. To this end, we examined the role of Cornin on human brain microvascular endothelial cell line (HBMEC) proliferation, invasion, and tube formation in in vitro. For study of mechanism, the phosphoinositide 3 kinase (PI3K)-Akt inhibitor LY294002, endothelial nitric oxide synthase (eNOS) inhibitor L-NAME, vascular endothelial growth factor (VEGF) antagonist sFlt-1 and VEGF receptor blocker SU-1498 were used. HMBEC proliferation was tested by MTT. Scratch adhesion test was used to assess the ability of invasion. A matrigel tube formation assay was performed to test capillary tube formation ability. PI3K-Akt-eNOS-VEGF pathway activation in HMBEC was tested by Western blot. Our data suggested that Cornin induces angiogenesis in vitro by increasing proliferation, invasion and tube formation. VEGF expression was increasing by Cornin and counteracted by VEGF antagonist sFlt-1, LY294002 and L-NAME in HMBEC. Tube formation was increased by Cornin and counteracted by VEGF receptor blocker-SU1498, LY294002 and L-NAME. It may be suggested that Cornin induces angiogenesis in vitro via a programmed PI3K/Akt/eNOS/VEGF signaling axis.
机译:在本研究中,我们试图阐明Cornin是否有助于诱导血管生成及其机制。为此,我们研究了Cornin在体外对人脑微血管内皮细胞系(HBMEC)增殖,侵袭和管形成的作用。为研究机理,使用了磷酸肌醇3激酶(PI3K)-Akt抑制剂LY294002,内皮型一氧化氮合酶(eNOS)抑制剂L-NAME,血管内皮生长因子(VEGF)拮抗剂sFlt-1和VEGF受体阻滞剂SU-1498。通过MTT测试HMBEC增殖。划痕附着力测试用于评估侵袭能力。进行基质胶管形成测定法以测试毛细管的形成能力。通过蛋白质印迹测试了HMBEC中PI3K-Akt-eNOS-VEGF途径的激活。我们的数据表明,Cornin通过增加增殖,侵袭和管形成来诱导体外血管生成。在HMBEC中,Cornin增加了VEGF的表达,并被VEGF拮抗剂sFlt-1,LY294002和L-NAME抵消。 Cornin增加了管的形成,并被VEGF受体阻滞剂SU1498,LY294002和L-NAME抵消。可能表明,Cornin通过编程的PI3K / Akt / eNOS / VEGF信号转导轴体外诱导血管生成。

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