Endothelial cells dysfunction induced by silica nanoparticles through oxidative stress via JNK/P53 and NF-κB pathways

The Risk Evaluation of Tungsten Oxide Nanoparticles in Cultured Rat Liver Cells for Its Safe Applications in Nanotechnology

“…p-JNK, p-c-Jun, p-p53, Bax, cleaved caspase-3 were significantly increased in the human umbilical vein endothelial cells (HUVECs) after exposure to silica nanoparticles, while Bcl-2 was dramatically suppressed. ROS scavenger could markedly inhibit the JNK, c-Jun and p53 activity, indicating that ROS could be upstream effectors of JNK and p53 (Liu and Sun 2010). Hsin et al (2008) found that nano silverinduced apoptosis was mediated by the ROS via JNK and p53 activation.…”

“…In the present study, MTT and LDH assays showed that the higher concentrations of WO 3 NPs decreased cell viability. Also, Liu and Sun (2010) found that exposure to high concentrations (100-200 ppm) of silica nanoparticles caused an increase of cytotoxicity in HUVECs. The LDH release was also increased by silica nanoparticles only at the highest concentration, indicating that exposure to high concentrations of silica nanoparticles could affect cell-membrane integrity and lead to cell death.…”

“…Oxidative stress is associated with protein and lipid oxidation, ultimately leading to a profound alteration in mitochondrial function (Pan et al 2009). Any change in the mitochondrial membrane permeability is known to be an early event in apoptosis (Liu and Sun 2010). It is known that ROS activates multiple signaling pathways, including mitogen activated protein kinase (MAPK) family and p53 expression signal transduction cascades (Simbula et al 2007).…”

“…It is known that ROS activates multiple signaling pathways, including mitogen activated protein kinase (MAPK) family and p53 expression signal transduction cascades (Simbula et al 2007). P53, Bax and Bcl-2 are also generally thought to be involved in mitochondria-dependent apoptosis (Liu and Sun 2010). p-JNK, p-c-Jun, p-p53, Bax, cleaved caspase-3 were significantly increased in the human umbilical vein endothelial cells (HUVECs) after exposure to silica nanoparticles, while Bcl-2 was dramatically suppressed.…”

“…ROS could also directly activate p53, most probably by the induction of DNA damage (Simbula et al 2007;Turkez and Togar 2010;Turkez and Geyikoglu 2010;Turkez et al 2012). Based on the results of Liu and Sun (2010), the following silica nanoparticles-mediated signaling pathways for apoptosis related events were proposed as ROS production (JNK/c-Jun phosphorylation), P53 activation, Bax up regulation and Bcl-2 down regulation. Previous studies showed that higher dose exposure to nanomaterials, including silica nanoparticles, titanium dioxide, zinc oxide, alumina nanoparticles led to proinflammatory and procoagulant responses in endothelial cells.…”