TY - JOUR
T1 - TiO 2 nanoparticles induce dysfunction and activation of human endothelial cells
AU - Montiel-Dávalos, Angélica
AU - Ventura-Gallegos, José Luis
AU - Alfaro-Moreno, Ernesto
AU - Soria-Castro, Elizabeth
AU - García-Latorre, Ethel
AU - Cabañas-Moreno, José Gerardo
AU - Del Pilar Ramos-Godinez, María
AU - López-Marure, Rebeca
PY - 2012/4/16
Y1 - 2012/4/16
N2 - Nanoparticles can reach the blood and cause inflammation, suggesting that nanoparticles-endothelial cells interactions may be pathogenically relevant. We evaluated the effect of titanium dioxide nanoparticles (TiO 2) on proliferation, death, and responses related with inflammatory processes such as monocytic adhesion and expression of adhesion molecules (E- and P-selectins, ICAM-1, VCAM-1, and PECAM-1) and with inflammatory molecules (tissue factor, angiotensin-II, VEGF, and oxidized LDL receptor-1) on human umbilical vein endothelial cells (HUVEC). We also evaluated the production of reactive oxygen species, nitric oxide production, and NF-κB pathway activation. Aggregates of TiO 2 of 300 nm or smaller and individual nanoparticles internalized into HUVEC inhibited proliferation strongly and induced apoptotic and necrotic death starting at 5 μg/cm 2. Besides, TiO 2 induced activation of HUVEC through an increase in adhesion and in expression of adhesion molecules and other molecules involved with the inflammatory process. These effects were associated with oxidative stress and NF-κB pathway activation. In conclusion, TiO 2 induced HUVEC activation, inhibition of cell proliferation with increased cell death, and oxidative stress. (Figure Presented).
AB - Nanoparticles can reach the blood and cause inflammation, suggesting that nanoparticles-endothelial cells interactions may be pathogenically relevant. We evaluated the effect of titanium dioxide nanoparticles (TiO 2) on proliferation, death, and responses related with inflammatory processes such as monocytic adhesion and expression of adhesion molecules (E- and P-selectins, ICAM-1, VCAM-1, and PECAM-1) and with inflammatory molecules (tissue factor, angiotensin-II, VEGF, and oxidized LDL receptor-1) on human umbilical vein endothelial cells (HUVEC). We also evaluated the production of reactive oxygen species, nitric oxide production, and NF-κB pathway activation. Aggregates of TiO 2 of 300 nm or smaller and individual nanoparticles internalized into HUVEC inhibited proliferation strongly and induced apoptotic and necrotic death starting at 5 μg/cm 2. Besides, TiO 2 induced activation of HUVEC through an increase in adhesion and in expression of adhesion molecules and other molecules involved with the inflammatory process. These effects were associated with oxidative stress and NF-κB pathway activation. In conclusion, TiO 2 induced HUVEC activation, inhibition of cell proliferation with increased cell death, and oxidative stress. (Figure Presented).
UR - http://www.scopus.com/inward/record.url?scp=84859816435&partnerID=8YFLogxK
U2 - 10.1021/tx200551u
DO - 10.1021/tx200551u
M3 - Artículo
C2 - 22352400
SN - 0893-228X
VL - 25
SP - 920
EP - 930
JO - Chemical Research in Toxicology
JF - Chemical Research in Toxicology
IS - 4
ER -