2 edition of Studies of activation and toxicity in cultured astrocytes. found in the catalog.
Studies of activation and toxicity in cultured astrocytes.
Mark R. Cookson
PhD thesis, Biological Sciences.
This study explores the role of the opioid growth factor (OGF)-OGF receptor (OGFr) axis in the proliferation of primary cultures of mouse cerebral astrocytes, as well as in spinal cord astrocytes of mice with experimental autoimmune encephalomyelitis (EAE), the animal model of multiple sclerosis. Characterized by their star-like shape astrocytes, also known as astroglia, represent the most abundant cell type in the brain. Closely linked to neurons with pivotal roles in synaptic activity and blood-brain barrier function, the study of astrocytes using in vitro co-culture models is becoming increasingly important in neuroscience research.
Thus, toxic effects of methylmercury (in the form of methylmercury chloride) and thiomersal are compared in cultured human astrocytes. In the brain mercuric mercury can be formed by in situ dealkylation of the organic Hg species 10 as well as oxidation of elemental Hg. 11 Therefore, cellular toxicity of mercuric Hg (in the form of HgCl 2) is. Importantly, studies have also demonstrated that α-synuclein released from neurons may be taken up by astrocytes, leading to reactive astrogliosis in an SH-SY5Y-astrocyte co-culture model, as well as in an α-synuclein transgenic mouse model. Taken together, these findings demonstrate that reactive astrogliosis is associated with PD by.
Another study, using electrochemical amperometry and frequency-modulated single-vesicle imaging, revealed that cultured astrocytes and freshly cut astrocytes from the rat hippocampus contain large vesicles (~ nm) that release glutamate in a “Kiss-and run” mode, in which the vesicular membrane rapidly attaches to and detaches from the. For example, cultured astrocytes subjected to oxygen and glucose deprivation showed a decrease in mitochondrial membrane potential, possibly caused by the mitochondrial permeability transition pore (mtPTP) opening, which leads to a loss of intramitochondrial contents, mitochondrial respiration and .
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Studies have shown that activated astrocytes release toxic molecules that cause neuronal damage. Considering our results on inhibitory effects of sinomenine on production of ROS and other factors from ADDL-treated astrocytic cells, we next asked whether this compound has any effect on indirect toxicity to hippocampal neuronal cells, HTAuthor: Deepali Singh, Apurva Agrawal, Chitra Mohinder Singh Singal, Hriday Shanker Pandey, Pankaj Seth, Shi.
Methods: The present study was intended to investigate whether pyroptosis, a highly inflammatory form of programmed cell death, participated in the bilirubin-mediated toxicity on cultured rat cortical astrocytes.
Further, VX, a potent and selective competitive drug, was used to inhibit the activation Cited by: A range of toxicity studies of astrocytes have been made using cultures of primary, subcultured, or permanent cell lines.
These have been extremely valuable in toxicity evaluation and understanding the mechanisms of action of a number of neurotoxic substances (see Cited by: 6.
Topics: 06T - Toxicology, poisons, Studies of activation and toxicity in cultured astrocytes [ Neurotoxicity, In vitro tests]Author: M.R Cookson. Europe PMC is an Elixir Core Data Resource Learn more ›.
Europe PMC is a service of the Europe PMC Funders' Group, in partnership with the European Bioinformatics Institute; and in cooperation with the National Center for Biotechnology Information at the U.S.
National Library of Medicine (NCBI/NLM).It includes content provided to the PMC International archive by participating by: 2. Reactive astrocytes are strongly induced by central nervous system (CNS) injury and disease, but their role is poorly understood.
Here we show that a subtype of reactive astrocytes. In this study, we investigated the effect of ferrous iron overload on AQP4 expression in cultured mouse astrocytes.
Primary cultures of astrocytes were exposed to ferrous iron, and the expression of AQP4 as well as the swelling of astrocyte were determined.
The present study indicates that PEA exerts differential effects against Aβ-induced toxicity in primary cultures of cortical neurons and astrocytes from non-Tg (wild-type) and 3xTg-AD mice. In particular, PEA displays protective properties in wild-type mouse cell cultures but not in 3xTg AD mouse neuronal cultured cells overexpressing Aβ.
The study investigated the protective effects of astrocytes on dopaminergic cells mediated by Wnt signaling. Our present study demonstrated that Wnt1 levels in U cells were decreased after 6-OHDA treatment and that coculture with Wnt1-overexpressing U astrocytes attenuated the toxic effect of 6-OHDA on dopaminergic SH-SY5Y cells.
The present study demonstrates that following Mn exposure, activation of the caspase-3 precursor protein is observed in cultured astrocytes.
Caspase-3 is significantly activated by Mn after exposure for 30 min, with peak activation occurring between 2 and 6 hours (Fig 4). In the present study, we found that HG-induced ROS production, which mediated astrocyte activation and cytokine production, suggesting that ROS may be involved in diabetes complications of CNS.
HG activates oxidative stress pathway in many types of cells, including neural stem cells (Jia et al.,Pandey et al.,Quan et al., ).
Oxidative stress plays a major role in cerebral ammonia toxicity and the pathogenesis of hepatic encephalopathy (HE). As shown in this study, ammonia induces a rapid RNA oxidation in cultured rat astrocytes, vital mouse brain slices, and rat brain in vivo.
This study compared the effects of toxicity of ethanol and its first metabolite acetaldehyde in rat astrocytes through cell viability and cell proliferation. The cells were treated with different concentrations of ethanol in the presence or absence of a catalase inhibitor 2-amino-1,2,4 triazole (AMT) or with different concentrations of.
Treatment of cultures with toll-like receptor (TLR) ligands or cytokines has become a popular approach to investigate astrocyte neuroinflammatory responses and to simulate the neural environment in various CNS disorders.
However, despite much effort, the mechanism of astrocyte activation such as the. OBJECTIVE: To study the toxicity of bilirubin in primary cultures of newborn rat cerebral cortical astrocytes.
STUDY DESIGN: Primary cultures of newborn rat astrocytes were incubated at bilirubin. Our previous studies established that induction of growth factor synthesis and neuroprotection by the β 2-adrenoceptor agonist clenbuterol in vitro and in vivo was associated with the activation of astrocytes, the major source of trophic factors in the the present study, we further investigated the specificity of β 2-adrenoceptor-mediated effects on astrocyte activation and.
Culture medium was changed after 24 h, and then replaced every 3 days. At confluence (10–14 days), cells that remained adhered to the flasks were astrocytes. The purity of the astrocyte cultures, ascertained by immunocytochemical staining with glial fibrillary acidic protein (GFAP), was >95% (data not shown).
Cell treatment. Cultured astrocytes were exposed to different concentrations of Fe 2+ (10, 25, 50 and μM) for certain periods (1, 3, 6, 12, and 24 h). (A) Fe 2+ had distinctive toxic effects on cultured astrocytes in a time- and dose-dependent manner.
n = 5 for each group. Values are mean ± SE. Studies of activation and toxicity in cultured astrocytes. Author: Cookson, Mark R. ISNI: Awarding Body: University of Salford Current Institution: University of Salford Date of Award: Availability of Full Text: Full text unavailable from EThOS.
The neuroprotective actions of cannabidiol and other cannabinoids were examined in rat cortical neuron cultures exposed to toxic levels of the excitatory neurotransmitter glutamate. Glutamate toxicity was reduced by both cannabidiol, a nonpsychoactive constituent of marijuana, and the psychotropic cannabinoid (−)Δ9-tetrahydrocannabinol (THC).
Astrocytes, also known collectively as astroglia, are characteristic star-shaped glial cells in the brain and spinal cord. They are the most | Explore the latest full-text research PDFs.
Microglia are activated by BDV-infected astrocytes. Our previous studies have demonstrated that the presence of astrocytes in mixed cultures appeared to be an important factor for BDV-associated activation of microglia .Specifically, in contrast to mixed neuron/astroglia/microglia cultures, co-culture of pure BDV-infected neurons and pure microglia does not produce microglia activation.
Importantly, senescent astrocytes were identified in aged and AD brain tissue, and other studies identified several factors that are responsible for inducing senescence in astrocytes [11, 15, 17]. These studies reported a link between an inflammatory environment and neurodegenerative diseases, but how astrocyte senescence might alter brain.