H-RN, a peptide derived from hepatocyte growth factor, inhibits corneal neovascularization by inducing endothelial apoptosis and arresting the cell cycle.
H-RN, a peptide derived from hepatocyte growth factor, inhibits corneal neovascularization by inducing endothelial apoptosis and arresting the cell cycle.
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H-RN 是一种源自肝细胞生长因子的肽，通过诱导内皮细胞凋亡和阻止细胞周期来抑制角膜新生血管形成
DOI：
10.1186/1471-2121-14-8
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发表时间：
2013-02-24
期刊：
影响因子：
--
通讯作者：
Xu X
中科院分区：
文献类型：
--
作者：
Sun Y;Su L;Wang Z;Xu Y;Xu X
背景本研究的目的是研究源自肝细胞生长因子 kringle 1 结构域 (HGF K1) 的新型肽 H-RN 在小鼠角膜新生血管模型中的抗血管生成活性。使用人脐静脉内皮细胞 (HUVEC) 体外评估 H-RN 对血管内皮生长因子 (VEGF) 刺激的细胞增殖、细胞迁移和内皮细胞管形成的抗血管生成作用，并使用小鼠角膜微袋测定进行体内评估。通过流式细胞术评估细胞凋亡和细胞周期停滞。以乱序肽作为阴性对照。结果H-RN能有效抑制VEGF刺激的HUVEC在Matrigel上的增殖、迁移和管形成，而乱序肽则无此作用。在小鼠角膜血管生成模型中，与没有这种活性的乱序肽相比，H-RN 显着抑制了 VEGF 刺激的血管生成。 VEGF 保护 HUVEC 免于凋亡，而 H-RN 抑制 VEGF 的这种保护作用。与对照处理的细胞相比，VEGF 显着增加了 S 期细胞的比例 (p<0.05)。 H-RN (1.5 mM) 处理诱导 G0/G1 期细胞积聚，而 S 期和 G2/M 期细胞比例较对照组显着下降 (p<0.05)。 结论 H-RN 在 HUVEC 和 VEGF 诱导的角膜新生血管小鼠模型中具有抗血管生成活性。 H-RN 的抗血管生成活性与细胞凋亡和细胞周期停滞相关，表明角膜抗血管生成治疗的潜在策略。
BackgroundThe goal of this study was to investigate the anti-angiogenic activity of a novel peptide H-RN, derived from the hepatocyte growth factor kringle 1 domain (HGF K1), in a mouse model of corneal neovascularization. The anti-angiogenic effect of H-RN on vascular endothelial growth factor (VEGF)-stimulated cell proliferation, cell migration and endothelial cell tube formation was assessedin vitrousing Human Umbilical Vein Endothelial Cells (HUVECs) andin vivousing a mouse cornea micropocket assay. Apoptosis and cell cycle arrest were assessed by flow cytometry. A scrambled peptide was used as a negative control.ResultsH-RN effectively inhibited VEGF-stimulated HUVEC proliferation, migration and tube formation on Matrigel, while a scrambled peptide exerted no effect. In the mouse model of corneal angiogenesis, VEGF-stimulated angiogenesis was significantly inhibited by H-RN compared to a scrambled peptide that had no such activity. VEGF protected HUVECs from apoptosis, while H-RN inhibited this protective effect of VEGF. VEGF significantly increased the proportion of cells in the S phase compared to control treated cells (p<0.05). Treatment with H-RN (1.5 mM) induced the accumulation of cells in G0/G1 phase, while the proportion of cells in the S phase and G2/M phase decreased significantly compared to control group (p<0.05).ConclusionsH-RN has anti-angiogenic activity in HUVECs and in a mouse model of VEGF-induced corneal neovascularization. The anti-angiogenic activity of H-RN was related to apoptosis and cell cycle arrest, indicating a potential strategy for anti-angiogenic treatment in the cornea.
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DOI：
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发表时间：
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影响因子：
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