Possible role of PAPR-1 in protecting human HaCaT cells against cytotoxicity of SiO2 nanoparticles

Abstract

Nano-SiO₂ materials play a significant role in the engineered nanomaterials (ENMs) field. The ease of their production as well as their relatively low cost has promoted the wide use of these products in many fields. Nano-SiO₂ exposure is known to cause severe DNA damage; however, the underlying mechanisms remain poorly understood. In a previous study, we found that nano-SiO₂ exposure regulate the expression of the poly(ADP-ribose) polymerases-1 (PARP-1), a pivotal DNA repair gene, in human HaCaT cells. Here, we employed lentivirus-mediated RNA interference (RNAi) to knock down PAPR-1 expression in HaCaT cells and explored the potential role of PARP-1 in nano-SiO₂ induced cytotoxicity. We found that nano-SiO₂ treatment of HaCaT cells causes decreased cell viability, increased apoptosis and DNA damage. Nano-SiO₂-treated HaCaT cells were also found to have slightly changed cell cycle distribution. Lentivirus-mediated PAPR-1 knockdown partially aggravated cytotoxicity and increased apoptosis induced by nano-SiO₂ treatment. Nano-SiO₂ had significant toxicity to human HaCaT cells and causes DNA damage. PAPR-1 knock-down cell line appears more sensitive to nano-SiO₂ than the control cells in DNA damage. The results suggest that PAPR-1 is involved in protecting cells from damage caused by nano-SiO₂.

Keywords: Cell transfection; DNA damage; Nano-SiO(2); Poly(ADP-ribose) polymerase.