https://nova.newcastle.edu.au/vital/access/ /manager/Index en-au 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:52762 Wed 28 Feb 2024 16:23:26 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:45247 Wed 26 Oct 2022 20:03:45 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:33581 Wed 21 Nov 2018 16:34:26 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:33579 Wed 19 Jan 2022 15:18:17 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:23930 Wed 17 Nov 2021 16:31:15 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:50144 Wed 13 Mar 2024 08:54:20 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:15202 Wed 11 Apr 2018 15:20:44 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14413 Wed 11 Apr 2018 14:45:30 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:30287 Wed 11 Apr 2018 12:31:05 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27925 Wed 10 Nov 2021 15:05:24 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:50139 Wed 05 Jul 2023 12:54:49 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:33578 Wed 04 Sep 2019 09:48:09 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:52190 Wed 04 Oct 2023 11:10:03 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:49081 Wed 03 May 2023 16:22:13 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:48116 Wed 01 Mar 2023 13:27:10 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:50026 Tue 27 Jun 2023 16:47:33 AEST ]]> https://nova.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://nova.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://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:45867 Tue 06 Dec 2022 10:38:10 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:33004 Tue 03 Sep 2019 18:17:54 AEST ]]> https://nova.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://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:41004 Thu 21 Jul 2022 10:51:14 AEST ]]> https://nova.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://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27924 Sat 24 Mar 2018 07:36:08 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27422 POS or Aldh1L1^POS astrocytes freshly isolated from uninjured, contralesional and lesioned hippocampus 4 days after entorhinal cortex lesion. To determine the Notch signaling competence of individual astrocytes, we measured the mRNA levels of Notch ligands and Notch1 receptor. We found that whereas most cultured and freshly isolated astrocytes were competent to receive Notch signals, only a minority of astrocytes were competent to send Notch signals. Injury increased the fraction of astrocyte subpopulation unable to send and receive Notch signals, thus resembling primary astrocytes in vitro. Astrocytes deficient of GFAP and vimentin showed decreased Notch signal sending competence and altered expression of Notch signaling pathway-related genes Dlk2, Notch1, and Sox2. Furthermore, we identified astrocyte subpopulations based on their mRNA and protein expression of nestin and HB-EGF. This study improves our understanding of astrocyte heterogeneity, and points to astrocyte cytoplasmic intermediate filaments as targets for neural cell replacement strategies.]]> Sat 24 Mar 2018 07:35:23 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:28444 -/-Vim^-/- mice, b-wave amplitudes were increased. Moreover, we found that Kir (inward rectifier K⁺) channel protein expression was reduced in the retinas of GFAP^-/-Vim^-/- mice and that Kir-mediated current amplitudes were lower in Müller glial cells isolated from these mice. Studies have shown that the IF system, in addition, is involved in the retinal response to injury and that attenuated Müller cell reactivity and reduced photoreceptor cell loss are observed in IF-deficient mice after experimental retinal detachment. We investigated whether the lack of IF proteins would affect cell survival in a retinal ischemia-reperfusion model. We found that although cell loss was induced in both genotypes, the number of surviving cells in the inner retina was lower in IF-deficient mice. Our findings thus show that the inability to produce GFAP and Vim affects normal retinal physiology and that the effect of IF deficiency on retinal cell survival differs, depending on the underlying pathologic condition.]]> Sat 24 Mar 2018 07:29:01 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27907 Sat 24 Mar 2018 07:24:37 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:28192 Sat 24 Mar 2018 07:23:54 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27576 Sat 24 Mar 2018 07:23:42 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:52857 Mon 30 Oct 2023 10:00:44 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:39237 -/-) mice were reported to exhibit subtle deficit in recall memory. Here, we subjected 3 months old male C3aR^-/- mice to a battery of behavioral tests and examined their brain morphology. We found that the C3aR^-/- mice exhibit a short-term memory deficit and increased locomotor activity, but do not show any signs of autistic behavior as assessed by self-grooming behavior. We also found regional differences between the C3aR^-/- and wild-type (WT) mice in the morphology of motor and somatosensory cortex, as well as amygdala and hippocampus. In summary, constitutive absence of C3aR signaling in mice leads to neurodevelopmental abnormalities that persist into adulthood and are associated with locomotive hyperactivity and altered cognitive functions.]]> Fri 27 May 2022 13:50:26 AEST ]]> https://nova.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 ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:47354 Fri 13 Jan 2023 13:20:00 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:41794 Fri 12 Aug 2022 12:17:18 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:51514 Fri 08 Sep 2023 12:03:44 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:37036 Fri 03 Dec 2021 10:32:41 AEDT ]]>