Silicon dioxide nanoparticles induce COX-2 expression through activation of STAT3 signaling pathway in HaCaT cells.

Silicon dioxide nanoparticles induce COX-2 expression through activation of STAT3 signaling pathway in HaCaT cells. Toxicol In Vitro. 2018 Jun 09;: Authors: Kundu J, Kim DH, Chae IG, Lee JK, Lee S, Jeong CH, Chun KS Abstract Silicon dioxide nanoparticles (SiO2-NPs) are widely used in biomedicines and consumer products, such as sunscreens and cosmetics. However, SiO2-NPs can cause adverse effects on human health, depending on the size and concentration of nanoparticles. The present study was aimed at investigating the molecular mechanism underlying SiO2-NPs-induced inflammation in human keratinocyte (HaCaT) cells. Incubation of HaCaT cells with SiO2-NPs induced the expression of cyclooxygenase-2 (COX-2) mRNA and protein. Treatment of cells with SiO2-NPs also induced the phosphorylation, DNA binding and the reporter gene activity of signal transducer and activator of transcription-3 (STAT3). Transfection of cells with STAT3 siRNA abrogated SiO2-NPs-induced COX-2 expression. Moreover, SiO2-NPs enhanced the phosphorylation of Janus activated kinase-2 (JAK2), Src and Akt. Pharmacological inhibition of either JAK2, Src or Akt abrogated SiO2-NPs-induced STAT3 transcriptional activity and the expression of COX-2. Treatment with LY294002 also attenuated SiO2-NPs-induced Src phosphorylation, however, JAK2 phosphorylation was not changed. In addition, SiO2-NPs generated reactive oxygen species (ROS) and treatment of N-acetyl cysteine (NAC) atte...
Source: Toxicology in Vitro - Category: Toxicology Authors: Tags: Toxicol In Vitro Source Type: research