https://nova.newcastle.edu.au/vital/access/ /manager/Index en-au 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:38877 Wed 23 Feb 2022 10:20:33 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:38875 Wed 23 Feb 2022 09:59:25 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:44648 2NPs) is on the increase, and so the number of studies dedicated to describing this material's biological effects. Previous studies have presented results indicating the controversial impact of TiO₂NPs on cell fate regarding death and survival. We speculate that this may be due to focusing on each of the subject cells as an isolated individual. In this study, we made a difference by looking at the subject cells as an interrelated population. Specifically, we exposed mesenchymal stem cells (MSCs) to TiO₂NPs and observed cell death and stimulation of proliferation among the cell population. Our data shows that the exposure to TiO₂NPs initiated autophagy, which led to an increase in extracellular Wnt protein levels and increased Wnt/GSK3β/β-catenin/cyclin D1 signalling in the cell population. Autophagy inhibitor repressed the effects of TiO₂NPs, which indicates that ß-catenin regulation was dependent on TiO₂NPs-induced autophagy. The inhibition of β-catenin resulted in dysregulation of cyclin D1 protein expression level. In conclusion, following exposure to TiO₂NPs, MSCs undergo autophagy, which induces cell proliferation among the cell population by upregulation of cyclin D1 through the Wnt/GSK3β/β-catenin pathway.]]> Wed 19 Oct 2022 09:00:38 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:30397 Tue 01 May 2018 09:18:50 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:44861 Thu 27 Oct 2022 13:56:38 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:37991 Thu 22 Jul 2021 16:00:46 AEST ]]> https://nova.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 ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:42364 Mon 22 Aug 2022 14:08:37 AEST ]]>