...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Angiogenesis >VEGF-C differentially regulates VEGF-A expression in ocular and cancer cells; promotes angiogenesis via RhoA mediated pathway
【24h】

VEGF-C differentially regulates VEGF-A expression in ocular and cancer cells; promotes angiogenesis via RhoA mediated pathway

机译：VEGF-C差异性调节眼和癌细胞中的VEGF-A表达。通过RhoA介导的途径促进血管生成

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Vascular angiogenesis is regulated by a number of cytokines of which vascular endothelial growth factor (VEGF)-A/and its receptor vascular endothelial growth factor receptor 2 (VEGFR2) play an indisputable role. Similarly lymphangiogenesis is regulated by VEGF-C and its receptor VEGFR3. Currently for treating vasculogenesis diseases such as proliferative retinopathies and cancer, a number of anti-VEGF-A therapies are approved for clinical use. Although clinical efficacies achieved are remarkable, they are found to be transitory in nature, followed by restoration of anti-VEGF therapy resistant angiogenesis. Recently the regulatory role of VEGF-C in initiating and potentiating neo-angiogenesis has been uncovered. Although the interactive nature of VEGF-A and C is known, the dynamics of their expression under knockdown conditions is yet to be established. Here in this study we have utilized siRNA to knockdown both VEGF-A and C either independently or in combination. Analysis of VEGF-A and C expression (only in cancer cell lines MCF7, A549 and H460 but not in the ocular cell line RPE19) has shown enhanced expression levels of VEGF-C with increase in knockdown of VEGF-A. However, VEGF-C knockdown has resulted in decreased expression levels of VEGF-A both in RPE19 and MCF7 cells in a dose dependent manner. In addition, VEGF-C knockdown also resulted in decreased expression of RhoA. Further, knockdown studies of RhoA even with supplementation of VEGF-C or A has resulted in decreased endothelial cell proliferation and stress fiber formation, indicating that VEGF-C does promote angiogenesis via RhoA mediated pathway.
机译：血管血管生成受多种细胞因子调节，其中血管内皮生长因子（VEGF）-A /及其受体血管内皮生长因子受体2（VEGFR2）发挥着无可争议的作用。同样，淋巴管生成受VEGF-C及其受体VEGFR3调节。当前，用于治疗血管增生性疾病例如增生性视网膜病和癌症的许多抗VEGF-A疗法被批准用于临床。尽管所取得的临床效果非常显着，但实际上发现它们是暂时的，随后恢复抗VEGF治疗的抗血管生成作用。最近，已经发现了VEGF-C在启动和增强新血管生成中的调节作用。尽管已知VEGF-A和C的相互作用性质，但在敲除条件下其表达的动力学尚待确定。在此研究中，我们已利用siRNA单独或组合地敲低VEGF-A和C。 VEGF-A和C表达的分析（仅在癌细胞系MCF7，A549和H460中，而在眼细胞系RPE19中没有）显示，VEGF-C的表达水平随VEGF-A的敲低而增加。但是，VEGF-C敲低已导致RPE19和MCF7细胞中VEGF-A的表达水平以剂量依赖性方式降低。另外，VEGF-C敲低也导致RhoA表达降低。此外，即使添加了VEGF-C或A，对RhoA的敲除研究也导致内皮细胞增殖减少和应力纤维形成，表明VEGF-C确实通过RhoA介导的途径促进了血管生成。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号