Research Topics
Genomes and GenesSpecies | Hideyuki TakeuchiSummaryAffiliation: Nagoya University Country: Japan Publications
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Detail Information
Publications
The direct and indirect effects of serofendic acid on neuroprotectionYukiko Doi
Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Furo-cho, Chikusa-ku, Nagoya 464-8601, Japan
Ann N Y Acad Sci 1086:91-103. 2006..Serofendic acid may be of use for the future therapeutic strategy against ischemic and degenerative neurological disorders...- Interferon-gamma induces microglial-activation-induced cell death: a hypothetical mechanism of relapse and remission in multiple sclerosisHideyuki Takeuchi
Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Furo cho, Chikusa ku, Nagoya 464 8601, Japan
Neurobiol Dis 22:33-9. 2006..Therefore, IFN-gamma may act on microglia as part of a self-limiting negative feedback system. The activation and subsequent death of microglia induced by IFN-gamma may play pivotal roles in the mechanism of MS relapse and remission... - Tumor necrosis factor-alpha induces neurotoxicity via glutamate release from hemichannels of activated microglia in an autocrine mannerHideyuki Takeuchi
Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Furo cho, Chikusa ku, Japan
J Biol Chem 281:21362-8. 2006..These drugs may give us a new therapeutic strategy against neurodegenerative diseases with minimum adverse side effects... 
Blockade of microglial glutamate release protects against ischemic brain injuryHideyuki Takeuchi
Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Nagoya, Japan
Exp Neurol 214:144-6. 2008..Thus, blockade of microglial glutamate release may be an effective therapeutic strategy against neurodegeneration after ischemic injury...- Neuritic beading induced by activated microglia is an early feature of neuronal dysfunction toward neuronal death by inhibition of mitochondrial respiration and axonal transportHideyuki Takeuchi
Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Furo cho, Chikusa ku, Nagoya 464 8601, Japan
J Biol Chem 280:10444-54. 2005..Blockage of NMDA receptors may be an effective therapeutic approach for neurodegenerative diseases... 
Blockade of gap junction hemichannel suppresses disease progression in mouse models of amyotrophic lateral sclerosis and Alzheimer's diseaseHideyuki Takeuchi
Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Furo cho, Chikusa ku, Nagoya, Japan
PLoS ONE 6:e21108. 2011..Hence, blockade of gap junction hemichannel may be potentially beneficial in treatment of neurodegenerative diseases...- Macrophage-induced neurotoxicity is mediated by glutamate and attenuated by glutaminase inhibitors and gap junction inhibitorsIzumi Yawata
Department of Neuroimmunology, Institute of Environmental Medicine, Nagoya University, Furo cho, Chikusa ku, Nagoya 464 8601, Japan
Life Sci 82:1111-6. 2008..Thus, these drugs may be effective therapeutic reagents for inflammatory, demyelinating, and ischemic brain diseases... - Interferon-beta is neuroprotective against the toxicity induced by activated microgliaShijie Jin
Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Furo cho, Chikusa ku, Nagoya, 464 8601, Japan
Brain Res 1179:140-6. 2007..These results suggest that IFN-beta may be a useful agent counteracting neurotoxicity associated with activated microglia... - Glutamate induces neurotrophic factor production from microglia via protein kinase C pathwayJianfeng Liang
Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Furo cho, Chikusa ku, Nagoya 464 8601, Japan
Brain Res 1322:8-23. 2010..These results suggest that microglia play a neuroprotective role during the excitotoxic state in neurodegenerative diseases... - The role of TNF-alpha and its receptors in the production of NGF and GDNF by astrocytesReiko Kuno
Department of Neuroimmunology, Institute of Environmental Medicine, Nagoya University, Furo-cho, Chikusa-ku, Nagoya 464-8601, Japan
Brain Res 1116:12-8. 2006..These results suggest that an autocrine loop involving TNF-alpha contributes to the production of neurotrophic factors in response to inflammation... - Excitatory amino acid transporter expression by astrocytes is neuroprotective against microglial excitotoxicityJianfeng Liang
Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Nagoya 464 8601, Japan
Brain Res 1210:11-9. 2008..These results revealed that astrocytic EAATs can counteract microglial glutamate-induced neuronal death whereas microglial EAATs are inconsequential to neurotoxicity and neuroprotection... - Blockade of glutamate release from microglia attenuates experimental autoimmune encephalomyelitis in miceJin Shijie
Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Nagoya, Japan
Tohoku J Exp Med 217:87-92. 2009..In EAE mice, treatment with CBX or DON also attenuated EAE clinical symptoms. Thus, blockade of glutamate release from activated microglia with CBX or DON may be an effective therapeutic strategy against neurodegeneration in MS... - X-Linked inhibitor of apoptosis protein is involved in mutant SOD1-mediated neuronal degenerationShinsuke Ishigaki
Department of Neurology, Nagoya University Graduate School of Medicine, Nagoya, Japan
J Neurochem 82:576-84. 2002..These results suggest that XIAP plays a role in the apoptotic mechanism in the progression of disease in mutant SOD1 Tg mice and holds therapeutic possibilities for FALS... - Interleukin-34 selectively enhances the neuroprotective effects of microglia to attenuate oligomeric amyloid-β neurotoxicityTetsuya Mizuno
Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Nagoya, Japan
Am J Pathol 179:2016-27. 2011..These findings support the idea that enhancement of the neuroprotective property of microglia by IL-34 may be an effective approach against oAβ neurotoxicity in AD... - Interleukin-25 expressed by brain capillary endothelial cells maintains blood-brain barrier function in a protein kinase Cepsilon-dependent mannerYoshifumi Sonobe
Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Furo cho, Chikusa ku, Nagoya 464 8601, USA
J Biol Chem 284:31834-42. 2009..These novel functions of IL-25 in maintaining BBB integrity may help us understand the pathophysiology of inflammatory brain diseases such as MS... - The neuroprotective effects of milk fat globule-EGF factor 8 against oligomeric amyloid β toxicityEndong Li
Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Furo cho, Chikusa ku, Nagoya 464 8601, Japan
J Neuroinflammation 9:148. 2012..However, the mechanisms by which microglia produce MFG-E8 and the precise functions of MFG-E8 are unknown... - Production and functions of IL-33 in the central nervous systemSatoko Yasuoka
Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Furo cho, Chikusa ku, Nagoya 464 8601, Japan
Brain Res 1385:8-17. 2011..It also enhances chemokines and nitric oxide production and phagocytosis by microglia. Thus, IL-33 produced in the CNS activates microglia and may function as a pro-inflammatory mediator in the pathophysiology of the CNS... - Production and functions of IL-17 in microgliaJun Kawanokuchi
Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Furo cho, Chikusaku, Nagoya 464 8601, Japan
J Neuroimmunol 194:54-61. 2008..Because microglia produce IL-1beta and IL-23, these cytokines may act in an autocrine manner to induce IL-17 expression in microglia, and thereby contribute to autoimmune diseases, such as MS, in the central nervous system... - Protective effects of nicergoline against neuronal cell death induced by activated microglia and astrocytesTetsuya Mizuno
Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Furo cho, Chikusa, Nagoya 464 8601, Japan
Brain Res 1066:78-85. 2005..Thus, nicergoline-mediated neuroprotection resulted primarily from the inhibition of inflammatory mediators and the upregulation of neurotrophic factors by glial cells... - Fractalkine attenuates excito-neurotoxicity via microglial clearance of damaged neurons and antioxidant enzyme heme oxygenase-1 expressionMariko Noda
Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Furo cho, Chikusa ku, Nagoya 464 8601, Japan
J Biol Chem 286:2308-19. 2011..These results suggest that sFKN secreted from glutamate-damaged neurons provides both phagocytotic and neuroprotective signals... - Autocrine activation of microglia by tumor necrosis factor-alphaReiko Kuno
Department of Neuroimmunology, Institute of Environmental Medicine, Nagoya University, Chikusa-ku, Nagoya 464-8601, Japan
J Neuroimmunol 162:89-96. 2005..These findings suggest the existence of a positive feedback loop in the activation of microglia via TNF-alpha. This autocrine loop may be involved in the prolonged activation of microglia... - Microglia activated with the toll-like receptor 9 ligand CpG attenuate oligomeric amyloid {beta} neurotoxicity in in vitro and in vivo models of Alzheimer's diseaseYukiko Doi
Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Japan
Am J Pathol 175:2121-32. 2009..We propose that CpG may be an effective therapeutic strategy for limiting oAbeta1-42 neurotoxicity in AD... - Immunoglobulin G(1) immune complex upregulates interferon-γ-induced nitric oxide production via ERK1/2 activation in murine microgliaBijay Parajuli
Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Furo cho, Chikusa ku, Nagoya, 464 8601, Japan
J Neuroimmunol 244:57-62. 2012..Collectively, these results indicate that IgG(1) immune complexes can exert immunomodulatory effects in various central nervous system disorders... - Chronological changes of CD4(+) and CD8(+) T cell subsets in the experimental autoimmune encephalomyelitis, a mouse model of multiple sclerosisYoshifumi Sonobe
Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Nagoya, Japan
Tohoku J Exp Med 213:329-39. 2007..Taking together, our data suggest that CD4(+) T cells are involved in the early phase of EAE, whereas CD8(+) T cells have a regulatory role in the later stage of EAE... - Gene expression profile of spinal motor neurons in sporadic amyotrophic lateral sclerosisYue-Mei Jiang
Department of Neurology, Nagoya University Graduate School of Medicine, Nagoya, Japan
Ann Neurol 57:236-51. 2005..The motor neuron-specific gene expression profile in sporadic ALS can provide direct information on the genes leading to neurodegeneration and neuronal death and are helpful for developing new therapeutic strategies... - Interferon-gamma directly induces neurotoxicity through a neuron specific, calcium-permeable complex of IFN-gamma receptor and AMPA GluR1 receptorTetsuya Mizuno
Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Furo cho, Chikusa ku, Nagoya, 464 8601 Japan
FASEB J 22:1797-806. 2008..These findings provide novel mechanisms of neuronal excitotoxicity, which may occur in both inflammatory and neurodegenerative diseases in the CNS... - Microglia express a functional receptor for interleukin-23Yoshifumi Sonobe
Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Furo cho, Chikusa ku, Nagoya, Aichi 464 8601, Japan
Biochem Biophys Res Commun 370:129-33. 2008..Thus, IL-23R expression does not discriminate peripheral macrophages from microglia. Moreover, since microglia produce IL-23, it may function in an autocrine manner to recruit inflammatory cells by inducing chemokine production... - The radical scavenger edaravone prevents oxidative neurotoxicity induced by peroxynitrite and activated microgliaMasahiro Banno
Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Furo-cho, Chikusa, Nagoya 464-8601, Japan
Neuropharmacology 48:283-90. 2005.... - Midkine inhibits inducible regulatory T cell differentiation by suppressing the development of tolerogenic dendritic cellsYoshifumi Sonobe
Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Nagoya 464 8601, Japan
J Immunol 188:2602-11. 2012..Taken together, these results suggest that MK aggravates EAE by suppressing DCreg development, thereby impairing the Treg population. Thus, MK is a promising therapeutic target for various autoimmune diseases... - GM-CSF increases LPS-induced production of proinflammatory mediators via upregulation of TLR4 and CD14 in murine microgliaBijay Parajuli
Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Furo cho, Chikusa ku, Nagoya, 464 8601, Japan
J Neuroinflammation 9:268. 2012..abstract:.. - Inhibition of midkine alleviates experimental autoimmune encephalomyelitis through the expansion of regulatory T cell populationJinyan Wang
Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Furo cho, Chikusa ku, Nagoya 464 8601, Japan
Proc Natl Acad Sci U S A 105:3915-20. 2008..These observations indicate that MK serves as a critical suppressor of Treg cell expansion, and inhibition of MK using RNA aptamers may provide an effective therapeutic strategy against autoimmune diseases, including multiple sclerosis... - Roles of glia-derived cytokines on neuronal degeneration and regenerationAkio Suzumura
Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Furo cho, Chikusa, Nagoya 464 8601, Japan
Ann N Y Acad Sci 1088:219-29. 2006.... - TGF-β induced by interleukin-34-stimulated microglia regulates microglial proliferation and attenuates oligomeric amyloid β neurotoxicityDi Ma
Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Furo cho, Chikusa ku, Nagoya 464 8601, Japan
Neurosci Lett 529:86-91. 2012..These findings suggest that TGF-β produced by IL-34-treated microglia is a negative regulator of microglial proliferation and enhances the neuroprotective property of microglia... - Production of IL-27 and other IL-12 family cytokines by microglia and their subpopulationsYoshifumi Sonobe
Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Furo-cho, Chikusa-ku, Nagoya 464-8601, Japan
Brain Res 1040:202-7. 2005..Primary microglia, but not their cell lines, also induce IL-12 and IL-23 upon above stimulation. Therefore, microglia may play a critical role initiating Th1 responses via producing IL-12 family cytokines in the brain... - Differential expression of inflammation- and apoptosis-related genes in spinal cords of a mutant SOD1 transgenic mouse model of familial amyotrophic lateral sclerosisTsuyoshi Yoshihara
Department of Neurology, Nagoya University Graduate School of Medicine, Nagoya, Japan
J Neurochem 80:158-67. 2002..Thus, ALS has paralleled other neurodegenerative disorders, such as Alzheimer's and prion diseases, in which the inflammatory process is believed to participate directly in neuronal death... - Hsp70 and Hsp40 improve neurite outgrowth and suppress intracytoplasmic aggregate formation in cultured neuronal cells expressing mutant SOD1Hideyuki Takeuchi
Department of Neurology, Nagoya University Graduate School of Medicine, 65 Tsurumai Cho, Showa Ku, Nagoya 466 8550, Japan
Brain Res 949:11-22. 2002..These findings may provide a basis for the utilization of HSPs in developing a treatment for FALS... - Mitochondrial localization of mutant superoxide dismutase 1 triggers caspase-dependent cell death in a cellular model of familial amyotrophic lateral sclerosisHideyuki Takeuchi
Department of Neurology, Nagoya University Graduate School of Medicine, 65 Tsurumai Cho, Showa Ku, Nagoya 466 8550, Japan
J Biol Chem 277:50966-72. 2002..These results suggest that the localization of mutant SOD1 in the mitochondria is critical in the pathogenesis of mutant SOD1-associated familial amyotrophic lateral sclerosis... - Dorfin prevents cell death by reducing mitochondrial localizing mutant superoxide dismutase 1 in a neuronal cell model of familial amyotrophic lateral sclerosisHideyuki Takeuchi
Department of Neurology, Nagoya University Graduate School of Medicine, 65 Tsurumai Cho, Showa Ku, Nagoya 466 8550, Japan
J Neurochem 89:64-72. 2004..These results suggest that reducing the accumulation of mutant SOD1 in the mitochondria may be a new therapeutic strategy for mutant SOD1-associated FALS, and that Dorfin may play a significant role in this... - Four-jointed is a Golgi kinase that phosphorylates a subset of cadherin domainsHiroyuki O Ishikawa
Howard Hughes Medical Institute, Waksman Institute and Department of Molecular Biology and Biochemistry, Rutgers University, Piscataway, NJ 08854, USA
Science 321:401-4. 2008..Our results indicate that Four-jointed regulates Fat signaling by phosphorylating cadherin domains of Fat and Dachsous as they transit through the Golgi...