Effects of nano-scaled particles on endothelial cell function in vitro: Studies on viability, proliferation and inflammation

Abstract

Recent studies give support for a connection between the presence of inorganic particles (of microm and nm size) in different organs and tissues and the development of inflammatory foci, called granulomas. As the potential source of particles (e.g. porcelain dental bridges) and the location of particle detection were topographically far apart, a distribution via the blood stream appears highly probable. Thus, endothelial cells, which line the inner surface of blood vessels, would come into direct contact with these particles, making particle-endothelial interactions potentially pathogenically relevant. The objective of this study was to evaluate the effects that five different nano-scaled particles (PVC, TiO2, SiO2, Co, Ni) have on endothelial cell function and viability. Therefore, human endothelial cells were exposed to different amounts of the above-mentioned particles. Although most particle types are shown to be internalised (except Ni-particles), only Co-particles possessed cytotoxic effects. Furthermore, an impairment of the proliferative activity and a pro-inflammatory stimulation of endothelial cells were induced by exposure to Co- and, to a lesser extent, by SiO2-particles. If a pro-inflammatory stimulation of endothelial cells occurs in vivo, a chronic inflammation could be a possible consequence.

Silica nanoparticles induce oxidative stress, inflammation, and endothelial dysfunction in vitro via activation of the MAPK/Nrf2 pathway and nuclear factor-κB signaling

“…17 There is evidence that SiNPs can induce reactive oxygen species (ROS), impairment of proliferative activity, inflammation, and cell death on vascular endothelial cells. [18][19][20] Our previous study confirmed that SiNPs caused deoxyribonucleic acid (DNA) damage via the Chk1-dependent G 2 /M-checkpoint signaling pathway on endothelial cells. 21 However, understanding of the molecular mechanisms involved in the cytotoxicity of SiNPs on endothelium is still limited.…”

Amorphous silica nanoparticles trigger vascular endothelial cell injury through apoptosis and autophagy via reactive oxygen species-mediated MAPK/Bcl-2 and PI3K/Akt/mTOR signaling

“…Endothelial cells could direct contact with the NPs, making NPs-endothelial interactions potentially pathogenically relevant. 6 Our previous studies showed that intratracheal-instilled SiNPs could pass through the alveolar-capillary barrier into systemic circulation, 7 and SiNPs triggered endothelial dysfunction. 8 However, knowledge on mechanisms of endothelial dysfunction is still limited.…”

Effects of titanium nanoparticles on adhesion, migration, proliferation, and differentiation of mesenchymal stem cells

“…15,16 Given the worldwide concerns about nanotoxicity in biomaterials, the potential cytotoxicity of titanium nanoparticles has also been investigated in different cell lines. Previous studies have demonstrated that titanium nanoparticles have negative effects on cells, including inflammatory reactions in endothelial cells, 17 damage to the DNA of human lymphoblastoid cells, 18 and induction of micronuclei and apoptosis in Syrian hamster embryo fibroblasts. 19 Other reports have shown that titanium dioxide (TiO 2 ) nanoparticles delivered to the abdominal cavity and liver in mice cause brain injury and liver damage, respectively.…”