Molecular mechanisms of EGFR activation by carbon nanoparticles in lung epithelial cells

Abstract

Background: Particulate air pollution induces pathogenic endpoints like proliferation, apoptosis, and pro-inflammatory reactions in lung epithelial cells. The activation of the epidermal growth factor receptor (EGFR) is a key step responsible for signaling events specific for these endpoints. Earlier experiments identified particle-derived reactive oxygen species (ROS) as one possible trigger eliciting the observed EGFR activation. As initial molecular mechanism responsible for the activation of this signaling event, we hypothesize a ligand-independent internalization of EGFR involving caveolin-1.