https://ogma.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:45247 Wed 26 Oct 2022 20:03:45 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:52190 Wed 04 Oct 2023 11:10:03 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:49081 Wed 03 May 2023 16:22:13 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:48562 Vim^-/-) display phenotypes reflecting reduced levels of cell activation and ability to counteract stress, for example, decreased reactivity of astrocytes after neurotrauma, decreased migration of astrocytes and fibroblasts, attenuated inflammation and fibrosis in lung injury, delayed wound healing, impaired vascular adaptation to nephrectomy, impaired transendothelial migration of lymphocytes and attenuated atherosclerosis. To address the role of vimentin in fat accumulation, we assessed the body weight and fat by dual-energy X-ray absorptiometry (DEXA) in Vim^-/- and matched wildtype (WT) mice. While the weight of 1.5-month-old Vim^-/- and WT mice was comparable, Vim^-/- mice showed decreased body weight at 3.5, 5.5 and 8.5 months (males by 19-22%, females by 18-29%). At 8.5 months, Vim^-/- males and females had less body fat compared to WT mice (a decrease by 24%, p < 0.05, and 33%, p < 0.0001, respectively). The body mass index in 8.5 months old Vim^-/- mice was lower in males (6.8 vs. 7.8, p < 0.005) and females (6.0 vs. 7.7, p < 0.0001) despite the slightly lower body length of Vim^-/- mice. Increased mortality was observed in adult Vim^-/- males. We conclude that vimentin is required for the normal accumulation of body fat.]]> Tue 21 Mar 2023 15:44:53 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:44249 GFAP^-/-Vim^-/-) exhibit increased post-traumatic synaptic plasticity and increased basal and post-traumatic hippocampal neurogenesis. Here we assessed the locomotor and exploratory behavior of GFAP^-/-Vim^-/- mice, their learning, memory and memory extinction, by using the open field, object recognition and Morris water maze tests, trace fear conditioning, and by recording reversal learning in IntelliCages. While the locomotion, exploratory behavior and learning of GFAP^-/-Vim^-/- mice, as assessed by object recognition, the Morris water maze, and trace fear conditioning tests, were comparable to wildtype mice, GFAP^-/-Vim^-/- mice showed more pronounced memory extinction when tested in IntelliCages, a finding compatible with the scenario of an increased rate of reorganization of the hippocampal circuitry.]]> Tue 11 Oct 2022 12:10:20 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:45867 Tue 06 Dec 2022 10:38:10 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:33582 SA/SA) leads to cytokinetic failures in fibroblasts and lens epithelial cells, resulting in chromosomal instability and increased expression of cell senescence markers. In this study, we investigated morphology, proliferative capacity, and motility of VIM^SA/SA astrocytes, and their effect on the differentiation of neural stem/progenitor cells. VIM^SA/SA astrocytes expressed less vimentin and more GFAP but showed a well-developed intermediate filament network, exhibited normal cell morphology, proliferation, and motility in an in vitro wound closing assay. Interestingly, we found a two- to fourfold increased neuronal differentiation of VIM^SA/SA neurosphere cells, both in a standard 2D and in Bioactive3D cell culture systems, and determined that this effect was neurosphere cell autonomous and not dependent on cocultured astrocytes. Using BrdU in vivo labeling to assess neural stem/progenitor cell proliferation and differentiation in the hippocampus of adult mice, one of the two major adult neurogenic regions, we found a modest increase (by 8%) in the fraction of newly born and surviving neurons. Thus, mutation of the serine sites phosphorylated in vimentin during mitosis alters intermediate filament protein expression but has no effect on astrocyte morphology or proliferation, and leads to increased neuronal differentiation of neural progenitor cells.]]> Tue 03 Sep 2019 17:59:31 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:41004 Thu 21 Jul 2022 10:51:14 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:19423 −/− Vim ^−/−) do not form cytoplasmic intermediate filaments. GFAP ^−/− Vim ^−/− mice develop larger infarcts after ischemic stroke (Li et al. in J Cereb Blood Flow Metab 28(3):468–481, 2008). Here, we attempted to analyze the underlying mechanisms using oxygen–glucose deprivation (OGD), an in vitro ischemia model, examining a potential link between astrocyte intermediate filaments and reactive oxygen species (ROS). We observed a reorganization of the intermediate filament network in astrocytes exposed to OGD. ROS accumulation was higher in GFAP ^−/− Vim ^−/− than wild-type astrocytes when exposed to OGD followed by reperfusion or when exposed to hydrogen peroxide. These results indicate that the elimination of ROS is impaired in the absence of the intermediate filament system. Compared to wild-type astrocytes, GFAP ^−/− Vim ^−/− astrocytes exposed to OGD and reperfusion exhibited increased cell death and conferred lower degree of protection to cocultured neurons. We conclude that the astrocyte intermediate filament system is important for the cell response to oxidative stress induced by OGD followed by reperfusion.]]> Sat 24 Mar 2018 07:51:56 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:47756 Nes^-/-) mice. We found that the proliferation of Nes^-/- neural stem cells was not altered, but neurogenesis in the hippocampal dentate gyrus of Nes^-/- mice was increased. Surprisingly, the proneurogenic effect of nestin deficiency was mediated by its function in the astrocyte niche. Through its role in Notch signaling from astrocytes to neural stem cells, nestin negatively regulates neuronal differentiation and survival; however, its expression in neural stem cells is not required for normal neurogenesis. In behavioral studies, nestin deficiency in mice did not affect associative learning but was associated with impaired long-term memory.]]> Fri 27 Jan 2023 10:25:04 AEDT ]]>