4.2 Article

Gold Nanoparticles Inhibit VEGF(165)-Induced Migration and Tube Formation of Endothelial Cells via the Akt Pathway

期刊

BIOMED RESEARCH INTERNATIONAL
卷 2014, 期 -, 页码 -

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HINDAWI LTD
DOI: 10.1155/2014/418624

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资金

  1. National Natural Science Foundation of China [30772131]
  2. National Key Basic Research and Development Program [2010CB833603]
  3. First Affiliated Hospital of Jinan University Scientific Foster Fund [511005004]
  4. Open Fund of the First Affiliated Hospital of Jinan University [511005026]
  5. Medical Scientific Research Foundation of Guangdong Province [A2011328]
  6. Key Laboratory of Functional Protein Research of Guangdong Higher Education Institutes, Jinan University

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The early stages of angiogenesis can be divided into three steps: endothelial cell proliferation, migration, and tube formation. Vascular endothelial growth factor (VEGF) is considered the most important proangiogenic factor; in particular, VEGF(165) plays a critical role in angiogenesis. Here, we evaluated whether gold nanoparticles (AuNPs) could inhibit the VEGF(165)-induced human umbilical vein endothelial cell (HUVEC) migration and tube formation. AuNPs and VEGF(165) were coincubated overnight at 4 degrees C, after which the effects on cell migration and tube formation were assessed. Cell migration was assessed using a modified wound-healing assay and a transwell chamber assay; tube formation was assessed using a capillary-like tube formation assay and a chick chorioallantoic membrane (CAM) assay. We additionally detected the cell surface morphology and ultrastructure using atomic force microscopy (AFM). Furthermore, Akt phosphorylation downstream of VEGFR-2/PI3K in HUVECs was determined in a Western blot analysis. Our study demonstrated that AuNPs significantly inhibited VEGF(165)-induced HUVEC migration and tube formation by affecting the cell surface ultrastructure, cytoskeleton and might have inhibited angiogenesis via the Akt pathway.

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