https://ogma.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:40957 Wed 20 Jul 2022 16:04:20 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:32076 Thu 27 Jan 2022 15:57:09 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:46649 2NP) following environmental exposure. At present, the consequences of TiO₂NP exposure in bone are not well known. The aim of this study was to investigate the effects of TiO₂NP on mesenchymal stem cells (MSCs) and potential underlying mechanisms. Mesenchymal bone marrow-derived cells were cultured and treated with various concentrations of TiO₂NP. Results showed that TiO₂NP incubation produced cytotoxicity as evidenced by reduced cell viability. Using Western blotting TiO₂NP was found to increase autophagy as determined by elevation in ratio of LC3-II from LC3-I without evidence of necrotic cell death as estimated by lactic dehydrogenase (LDH) level. TiO2NP produced a rise in intracellular reactive oxygen species (ROS) levels. The observed alterations in autophagy and oxidant stress were associated with upregulation of protein expression of p38, JNK, and ERK. Data indicate that TiO₂NP-mediated decrease in MSC survival involves a complex series of events associated stimulation of mitogen-activated protein kinase (MAPK) pathway and consequent autophagy and oxidative damage.]]> Mon 28 Nov 2022 17:22:23 AEDT ]]>