Regulation of c-Myc and Bcl-2 Induced Apoptosis of Human Bronchial Epithelial Cells by Zinc Oxide Nanoparticles
Zinc oxide nanoparticles (ZnO NPs) are increasingly recognized for their cytotoxicity, whereas little is known about the toxicity mechanisms of ZnO NPs in human cells. To explore the possible molecular mechanisms for apoptosis induced by ZnO NPs, we investigated the relevant apoptotic signaling in human bronchial epithelial (16HBE) cells. ZnO NPs were found to induce intracellular reactive oxygen species (ROS) generation accompanied with the mitochondrial membrane potential (MMP, Δψ m) reduction in 16HBE cells. Further, the expressions of two key apoptotic trigger regulators were determined by quantitative real time PCR and Western blot analysis. It demonstrated that following the exposure of 16HBE cells to ZnO NPs, both levels of mRNA and protein expression of c-Myc were significantly up-regulated, whereas the expressions of Bcl-2 mRNA and protein were down-regulated. Our results suggested that apoptosis induced by ZnO NPs might primarily involve the regulations of c-Myc and Bcl-2 gene expressions besides decline of MMP in 16HBE cells.
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Document Type: Research Article
Publication date: 01 August 2012
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- Journal of Biomedical Nanotechnology (JBN) is a peer-reviewed multidisciplinary journal providing broad coverage in all research areas focused on the applications of nanotechnology in medicine, drug delivery systems, infectious disease, biomedical sciences, biotechnology, and all other related fields of life sciences.
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