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

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 e...

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Detalles Bibliográficos
Autores principales: Pan, Yunlong, Wu, Qing, Qin, Li, Cai, Jiye, Du, Bin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4058682/
https://www.ncbi.nlm.nih.gov/pubmed/24987682
http://dx.doi.org/10.1155/2014/418624
Descripción
Sumario: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°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.