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Статті в журналах з теми "Astrocytes Neuroinflammation"
Michinaga, Shotaro, and Yutaka Koyama. "Pathophysiological Responses and Roles of Astrocytes in Traumatic Brain Injury." International Journal of Molecular Sciences 22, no. 12 (June 15, 2021): 6418. http://dx.doi.org/10.3390/ijms22126418.
Повний текст джерелаLindman, Marissa, Juan Angel, Kimberly Newman, Colm Atkins, and Brian Daniels. "Astrocytic RIPK3 confers protection against deleterious neuroinflammation during Zika virus infection." Journal of Immunology 208, no. 1_Supplement (May 1, 2022): 163.27. http://dx.doi.org/10.4049/jimmunol.208.supp.163.27.
Повний текст джерелаZulfiqar, Shadaan, Pretty Garg, and Katja Nieweg. "Contribution of astrocytes to metabolic dysfunction in the Alzheimer’s disease brain." Biological Chemistry 400, no. 9 (August 27, 2019): 1113–27. http://dx.doi.org/10.1515/hsz-2019-0140.
Повний текст джерелаKarpuk, Nikolay, Maria Burkovetskaya, and Tammy Kielian. "Neuroinflammation alters voltage-dependent conductance in striatal astrocytes." Journal of Neurophysiology 108, no. 1 (July 1, 2012): 112–23. http://dx.doi.org/10.1152/jn.01182.2011.
Повний текст джерелаPhillips, Emma C., Cara L. Croft, Ksenia Kurbatskaya, Michael J. O’Neill, Michael L. Hutton, Diane P. Hanger, Claire J. Garwood, and Wendy Noble. "Astrocytes and neuroinflammation in Alzheimer's disease." Biochemical Society Transactions 42, no. 5 (September 18, 2014): 1321–25. http://dx.doi.org/10.1042/bst20140155.
Повний текст джерелаZhang, Xiang, Hao Yao, Qingqing Qian, Nana Li, Wenjie Jin, and Yanning Qian. "Cerebral Mast Cells Participate In Postoperative Cognitive Dysfunction by Promoting Astrocyte Activation." Cellular Physiology and Biochemistry 40, no. 1-2 (2016): 104–16. http://dx.doi.org/10.1159/000452528.
Повний текст джерелаHansson, Elisabeth. "Long-term pain, neuroinflammation and glial activation." Scandinavian Journal of Pain 1, no. 2 (April 1, 2010): 67–72. http://dx.doi.org/10.1016/j.sjpain.2010.01.002.
Повний текст джерелаGayen, Manoshi, Manish Bhomia, Nagaraja Balakathiresan, and Barbara Knollmann-Ritschel. "Exosomal MicroRNAs Released by Activated Astrocytes as Potential Neuroinflammatory Biomarkers." International Journal of Molecular Sciences 21, no. 7 (March 27, 2020): 2312. http://dx.doi.org/10.3390/ijms21072312.
Повний текст джерелаHe, Tingting, Guo-Yuan Yang, and Zhijun Zhang. "Crosstalk of Astrocytes and Other Cells during Ischemic Stroke." Life 12, no. 6 (June 17, 2022): 910. http://dx.doi.org/10.3390/life12060910.
Повний текст джерелаTakahashi, Shinichi, and Kyoko Mashima. "Neuroprotection and Disease Modification by Astrocytes and Microglia in Parkinson Disease." Antioxidants 11, no. 1 (January 17, 2022): 170. http://dx.doi.org/10.3390/antiox11010170.
Повний текст джерелаДисертації з теми "Astrocytes Neuroinflammation"
Brothers, Holly M. "Neuroinflammation, Glutamate Regulation and Memory." The Ohio State University, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=osu1363603410.
Повний текст джерелаWu, Celina. "Dual agonist-antagonist functions of FTY720 influence neuroinflammation-relevant responses in human astrocytes." Thesis, McGill University, 2012. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=110720.
Повний текст джерелаLes astrocytes sont les cellules gliales les plus abondantes du système nerveux central (SNC). Leur grande expression en filaments intermédiaires, la protéine acide fibrillaire gliale (GFAP), est une caractéristique permettant leur identification. Les astrocytes sont d'importants contributeurs aux événements biochimiques du SNC et jouent un rôle clé dans le processus de régulation des dommages et de la guérison du SNC. Sous des conditions d'inflammation chronique, tel la Sclérose en Plaques (SP), les astrocytes subissent des changements pathophysiologiques causant l'astrogliose (Liberto, Albrecht et al. 2004; Sidoryk-Wegrzynowicz, Wegrzynowicz et al. 2011). Ce mécanisme de cicatrisation est commun dans la SP et un nouvel agent thérapeutique, FTY720 (fingolimod, Gilenya™) démontre des effets protecteurs du SNC en prévenant l'évolution de l'astrogliose. (Choi, Gardell et al. 2011). FTY720 est un agent thérapeutique récemment approuvé pour traiter la SP. Il est administré oralement et a la capacité d'accéder au SNC. Une fois en place dans ce système, cet agent entre en contact direct avec le récepteur sphingosine-1-phosphate (S1PR) sur les astrocytes. Les réponses des astrocytes en réaction aux signaux générés par ce récepteur sont reliées à la pathologie de la SP. Cette thèse examine les signaux engendrés par FTY720 ainsi que ses fonctions sur les astrocytes humains primaires. Nous avons utilisé des astrocytes isolés à partir de SNC humains fœtaux pour examiner les réponses neuro-inflammatoires générées par l'administration quotidienne de FTY720. FTY720 agit initialement comme un agoniste en activant le récepteur S1P, mais il agit également comme un antagoniste en causant l'internalisation et la dégradation de ce récepteur. Nous avons examiné ces deux phénomènes de façon à savoir s'ils agissent en concert. Nous affirmons qu'un récepteur internalisé par FTY720 continue de générer des signaux pour une période de temps prolongée (heures). Une addition simple de FTY720 désensibilise l'astrocyte, pour une période de >24h, au signal de phosphorylation de ERK (pERK) qui est généré par le récepteur extracellulaire. Cette période réfractaire du signal de transduction de pERK fût maintenue dans les astrocytes traités quotidiennement avec FTY720, sinon le signal pERK reparaît 72 heures après le traitement initial. De plus, la désensibilisation du récepteur fût reliée à l'absence de réponse proliférative induite par le ligand naturel sphingosine-1-phosphate (S1P). Nous avons aussi démontré que le traitement quotidien des astrocytes avec FTY720 atténue la capacité de IL-1β à activer les voies moléculaires sensibles au calcium. Le traitement quotidien avec FTY720 n'inhibe pas les signaux de pERK lorsque les astrocytes sont stimulés à l'aide de sérum, ni la sécrétion de IL-6 ou de IP-10 lorsqu'ils sont stimulés avec IL-1β. Nos résultats suggèrent que l'exposition quotidienne à FTY720 agit comme un antagoniste aux stimuli extérieur (tel le ligand naturel S1P) ainsi qu'un agoniste lorsque le récepteur est internalisé (inhibe la mobilisation du calcium lorsqu'exposé à IL-1β).
Hoskins, Andrew. "The Role of IRF1 in the Brain and in Adaptive Responses of Astrocytes." VCU Scholars Compass, 2019. https://scholarscompass.vcu.edu/etd/5757.
Повний текст джерелаClement, Tifenn. "Contribution of astrocytes in brain vulnerability after juvenile mild traumatic brain injury." Thesis, Bordeaux, 2020. http://www.theses.fr/2020BORD0141.
Повний текст джерелаAstrocytes are crucial for various physiological functions in the brain such as homeostasis, metabolism, neurovascular coupling or neurotransmission regulation. In injuries, astrocytes become reactive and have a crucial role in the neuroinflammatory response. This reactivity is heterogeneous and depends on many parameters such as the type and severity of insult, astrocyte proximity to insult, or state of brain maturity. However, the specific response of astrocytes to mild traumatic brain injury (TBI) in the developmental context has never been studied yet. Mild TBI is the leading cause of emergency department visits in the pediatric population. A significant proportion of mild TBI pediatric patients will suffer of long-lasting cognitive and emotional impairments but the underlying cellular and molecular mechanisms are still poorly understood. Astrocytes might take part to this vulnerability and be partly responsible for the long-term consequences.We investigated astrocyte response to juvenile mild TBI and hypothesized that: (1) astrocytes display a specific pattern of reactivity evolving over time and brain development; and that (2) astrocytes reactivity differs when the TBI is preceded by an early systemic inflammation inducing a priming of astrocytes, with a different neuroinflammatory and vascular response to juvenile mild TBI, impacting the brain vulnerability and long-term outcome.We have shown that:(1) Reactive astrocytes express a specific spatiotemporal reactivity pattern even at distance from the injury site, in terms of intermediate filaments expression and morphological evolution, and that structural alterations are observed in brain imaging on the long-term after juvenile mild TBI.(2) When the juvenile mild TBI is preceded by perinatal systemic inflammation, astrocytes express a different reactivity phenotype considered as a state of transition towards scar-forming astrocytes, with increased metabolism and extracellular matrix-related gene changes, associated to morphological alterations sustaining over time and delayed over-expression of VEGF, resulting in the absence of vascular alterations induced by TBI alone.This work brings new insights in the specificities of astrocyte reactivity and in the pathophysiology of vulnerability after juvenile mild TBI, opening possibilities for novel targets for therapeutics
Phillips, Emma Claire. "Investigating the contribution of astrocytes and neuroinflammation to pathological tau changes in Alzheimer's disease." Thesis, King's College London (University of London), 2017. https://kclpure.kcl.ac.uk/portal/en/theses/investigating-the-contribution-of-astrocytes-and-neuroinflammation-to-pathological-tau-changes-in-alzheimers-disease(d96f6fa6-6870-4461-82b2-0a19d5507eab).html.
Повний текст джерелаDorey, Evan J. "Apolipoprotein E Isoforms Differentially Regulate Amyloid-β Stimulated Inflammation in Rat and Mouse Astrocytes". Thesis, Université d'Ottawa / University of Ottawa, 2012. http://hdl.handle.net/10393/23581.
Повний текст джерелаCeyzériat, Kelly. "Modulation de la réactivité astrocytaire par ciblage de la voie JAK2-STAT3 : conséquences dans des modèles murins de la maladie d’Alzheimer." Thesis, Université Paris-Saclay (ComUE), 2017. http://www.theses.fr/2017SACLS556/document.
Повний текст джерелаAstrocytes are emerging as key players in brain physiology. In Alzheimer’s disease (AD), astrocytes become reactive. Astrocyte reactivity (AR) is essentially characterized by morphological changes. But how the normal supportive functions of astrocytes are changed by their reactive state is unclear. Moreover, signaling cascades leading to AR are not yet determined. In this study, we aim to: 1/ demonstrate the JAK2-STAT3 pathway (Janus Kinase 2 - Signal Transducer and Activator of Transcription 3) is responsible for AR in neurodegenerative diseases ; 2/ understand the contribution of reactive astrocytes to molecular, cellular and functional alterations in AD. We already reported that the JAK2- STAT3 pathway is a central cascade for AR (Ben Haim et al., 2015). Here, we demonstrate, with new molecular tools based on viral vectors, that this pathway is necessary and sufficient to AR. Our results also show that the modulation of AR in two AD mouse models (APP/PS1dE9 and 3xTg-AD mice) influence several pathological hallmarks, but in a context-dependent manner. Overall, this work has generated new original tools to study reactive astrocytes in situ and it underlines the importance and complexity of their functions in neurodegenerative diseases
Frakes, Ashley E. "The Role of Neuroinflammation in the Pathogenesis of Amyotrophic Lateral Sclerosis." The Ohio State University, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=osu1417649954.
Повний текст джерелаGuillot, Flora. "Caractérisation de l'infiltrat lymphocytaire et de la réactivité astrocytaire dans un modèle de neuroinflammation autoimmune." Nantes, 2014. https://archive.bu.univ-nantes.fr/pollux/show/show?id=eba4b03e-07fe-4198-a88d-16cbb5f7f5eb.
Повний текст джерелаMultiple sclerosis (MS) is an autoimmune, demyelinating and degenerative disease of the central nervous system (CNS), in which astrocyte reactivity is considered an important player. The CD4 T cell response is strongly associated with development of MS and its animal models such as experimental autoimmune encephalomyelitis (EAE). Recent data suggest that anti-myelin CD8 T cells may be also implicated as CD8 T cells are abundant in MS lesions. To better understand the contribution of pathogenic CD8 T cells, two animal models that have been described were evaluated. The first one consists of mice immunized with a specific CD8 T cell myelin epitope (MOG37-46). Mice develop mild EAE with CD4 T overwhelming CD8 T cells in CNS. Boosting the CD8 immune response increased slightly the CD8/CD4 ratio in the CNS. The second model is based on the adoptive transfer of anti-HemAgglutinin (HA) CD8 T cells in DKI transgenic mice, which express HA by oligodendrocytes. Only irradiation (2Gy) of DKI mice allowed CNS infiltration of CD8 T cells but without apparent clinical signs. These results are discussed in light of recent literature. In parallel, we characterized the astrocyte reactivity in a classical EAE to better define the implication of astrocytes in the pathology. For this, we used for the first time in this model laser-capture microdissection to isolate white matter astrocytes in spinal cord lesion. Selected transcript profiling analysis revealed astrocytic expression of pro-inflammatory mediators and enzymes involved in oestrogen metabolism. These results give new clues for targeting glial reactivity in neuroinflammatory disorders such as MS
Ben, Haim Lucile. "Modulation of the JAK2/STAT3 pathway in vivo : understanding reactive astrocyte functional features and contribution to neurodegenerative diseases." Thesis, Paris 6, 2014. http://www.theses.fr/2014PA066534/document.
Повний текст джерелаAstrocyte reactivity is a hallmark of pathological conditions in the CNS including neurodegenerative diseases (ND) such as Alzheimer’s (AD) and Huntington’s (HD) diseases. Reactive astrocytes (RA) are identified by morphological changes but their functional features and influence on neurons are poorly understood, especially in ND. Therefore, we aimed at 1) identifying the signaling cascades involved in astrocyte reactivity in ND, 2) evaluating RA contribution to disease phenotype in ND models and 3) deciphering RA functional features. The JAK2/STAT3 pathway is a known trigger of astrocyte reactivity in CNS injuries. Here, we show that this pathway is a common inducer of astrocyte reactivity in AD and HD models. We developed new viral vectors to target this cascade in astrocytes and manipulate astrocyte reactivity in vivo. We used these vectors to determine the contribution of RA to neuronal dysfunction in HD mouse models. We found that RA do not primarily influence disease phenotype in HD. Last, we targeted the JAK2/STAT3 pathway in WT mice to characterize RA functional features in vivo. We show RA undergo transcriptional changes of numerous genes involved in metabolism, protein degradation pathways and immune response. Moreover, we show that astrocyte reactivity alters synaptic plasticity in the mouse hippocampus. Our results identify the JAK2/STAT3 pathway as a central cascade for astrocyte reactivity. The viral vectors developed in this project represent powerful tools to decipher the roles of RA in various ND models and to characterize RA functional features in vivo. Better understanding RA functions may lead to the identification of new therapeutic targets for ND
Частини книг з теми "Astrocytes Neuroinflammation"
Meares, Gordon P., and Etty N. Benveniste. "Inflammation and the Pathophysiology of Astrocytes in Neurodegenerative Diseases." In Neuroinflammation and Neurodegeneration, 61–80. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1071-7_4.
Повний текст джерелаTewari, Manju, and Pankaj Seth. "Astrocytes in Neuroinflammation and Neuronal Disorders: Shifting the Focus from Neurons." In Inflammation: the Common Link in Brain Pathologies, 43–70. Singapore: Springer Singapore, 2016. http://dx.doi.org/10.1007/978-981-10-1711-7_3.
Повний текст джерелаKriz, Jasna. "Neuron–Astrocyte Interactions in Neuroinflammation." In Advances in Neurobiology, 75–89. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-8313-7_5.
Повний текст джерелаMishra, Pooja Shree, Anu Mary Varghese, K. Vijayalakshmi, Veeramani Preethish-Kumar, Kiran Polavarapu, Seena Vengalil, Atchayaram Nalini, Phalguni Anand Alladi, Talakad N. Sathyaprabha, and Trichur R. Raju. "Interplay Between Microglia and Astrocytes During Neuroinflammation: Lessons Learnt from In Vitro and In Vivo Models of Sporadic Amyotrophic Lateral Sclerosis." In The Biology of Glial Cells: Recent Advances, 439–57. Singapore: Springer Singapore, 2022. http://dx.doi.org/10.1007/978-981-16-8313-8_16.
Повний текст джерелаFacci, Laura, Massimo Barbierato, and Stephen D. Skaper. "Astrocyte/Microglia Cocultures as a Model to Study Neuroinflammation." In Neurotrophic Factors, 127–37. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7571-6_10.
Повний текст джерелаBir, Shyamal C., Oleg Y. Chernyshev, and Alireza Minagar. "Roles of Macrophages and Astrocytes in Pathogenesis of Multiple Sclerosis." In Neuroinflammation, 517–28. Elsevier, 2018. http://dx.doi.org/10.1016/b978-0-12-811709-5.00028-4.
Повний текст джерелаMunir, Farwa, Nida Islam, Muhammad Hassan Nasir, Zainab Anis, Shahar Bano, Shahzaib Naeem, Atif Amin Baig, and Zaineb Sohail. "Impact of Hypoxia on Astrocyte Induced Pathogenesis." In Astrocytes in Brain Communication and Disease [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.106263.
Повний текст джерелаBenarroch, Eduardo E. "Microglia and Neuroinflammation." In Neuroscience for Clinicians, edited by Eduardo E. Benarroch, 402–15. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780190948894.003.0022.
Повний текст джерелаCrespo-Castrillo, Andrea, Maria Angeles Arevalo, Luis M. Garcia-Segura, and Natalia Yanguas-Casás. "Estrogenic Regulation of Glia and Neuroinflammation." In Estrogens and Memory, 96–116. Oxford University Press, 2020. http://dx.doi.org/10.1093/oso/9780190645908.003.0008.
Повний текст джерелаVesce, Sabino, Daniela Rossi, Liliana Brambilla, and Andrea Volterra. "Glutamate Release from Astrocytes in Physiological Conditions and in Neurodegenerative Disorders Characterized by Neuroinflammation." In International Review of Neurobiology, 57–71. Elsevier, 2007. http://dx.doi.org/10.1016/s0074-7742(07)82003-4.
Повний текст джерела