Hideyuki Takeuchi

Summary

Affiliation: Nagoya University
Country: Japan

Publications

  1. ncbi request reprint The direct and indirect effects of serofendic acid on neuroprotection
    Yukiko 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
  2. ncbi request reprint Neuritic beading induced by activated microglia is an early feature of neuronal dysfunction toward neuronal death by inhibition of mitochondrial respiration and axonal transport
    Hideyuki 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
  3. ncbi request reprint Tumor necrosis factor-alpha induces neurotoxicity via glutamate release from hemichannels of activated microglia in an autocrine manner
    Hideyuki Takeuchi
    Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Furo cho, Chikusa ku, Japan
    J Biol Chem 281:21362-8. 2006
  4. ncbi request reprint Interferon-gamma induces microglial-activation-induced cell death: a hypothetical mechanism of relapse and remission in multiple sclerosis
    Hideyuki 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
  5. doi request reprint Blockade of microglial glutamate release protects against ischemic brain injury
    Hideyuki Takeuchi
    Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Nagoya, Japan
    Exp Neurol 214:144-6. 2008
  6. pmc Blockade of gap junction hemichannel suppresses disease progression in mouse models of amyotrophic lateral sclerosis and Alzheimer's disease
    Hideyuki Takeuchi
    Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Furo cho, Chikusa ku, Nagoya, Japan
    PLoS ONE 6:e21108. 2011
  7. doi request reprint Macrophage-induced neurotoxicity is mediated by glutamate and attenuated by glutaminase inhibitors and gap junction inhibitors
    Izumi Yawata
    Department of Neuroimmunology, Institute of Environmental Medicine, Nagoya University, Furo cho, Chikusa ku, Nagoya 464 8601, Japan
    Life Sci 82:1111-6. 2008
  8. ncbi request reprint Interferon-beta is neuroprotective against the toxicity induced by activated microglia
    Shijie 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
  9. doi request reprint Glutamate induces neurotrophic factor production from microglia via protein kinase C pathway
    Jianfeng 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
  10. ncbi request reprint Blockade of glutamate release from microglia attenuates experimental autoimmune encephalomyelitis in mice
    Jin Shijie
    Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Nagoya, Japan
    Tohoku J Exp Med 217:87-92. 2009

Collaborators

Detail Information

Publications42

  1. ncbi request reprint The direct and indirect effects of serofendic acid on neuroprotection
    Yukiko 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...
  2. ncbi request reprint Neuritic beading induced by activated microglia is an early feature of neuronal dysfunction toward neuronal death by inhibition of mitochondrial respiration and axonal transport
    Hideyuki 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...
  3. ncbi request reprint Tumor necrosis factor-alpha induces neurotoxicity via glutamate release from hemichannels of activated microglia in an autocrine manner
    Hideyuki 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...
  4. ncbi request reprint Interferon-gamma induces microglial-activation-induced cell death: a hypothetical mechanism of relapse and remission in multiple sclerosis
    Hideyuki 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...
  5. doi request reprint Blockade of microglial glutamate release protects against ischemic brain injury
    Hideyuki 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...
  6. pmc Blockade of gap junction hemichannel suppresses disease progression in mouse models of amyotrophic lateral sclerosis and Alzheimer's disease
    Hideyuki 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...
  7. doi request reprint Macrophage-induced neurotoxicity is mediated by glutamate and attenuated by glutaminase inhibitors and gap junction inhibitors
    Izumi 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...
  8. ncbi request reprint Interferon-beta is neuroprotective against the toxicity induced by activated microglia
    Shijie 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...
  9. doi request reprint Glutamate induces neurotrophic factor production from microglia via protein kinase C pathway
    Jianfeng 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...
  10. ncbi request reprint Blockade of glutamate release from microglia attenuates experimental autoimmune encephalomyelitis in mice
    Jin 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...
  11. doi request reprint Excitatory amino acid transporter expression by astrocytes is neuroprotective against microglial excitotoxicity
    Jianfeng 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...
  12. ncbi request reprint X-Linked inhibitor of apoptosis protein is involved in mutant SOD1-mediated neuronal degeneration
    Shinsuke 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...
  13. ncbi request reprint The role of TNF-alpha and its receptors in the production of NGF and GDNF by astrocytes
    Reiko 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...
  14. pmc GM-CSF increases LPS-induced production of proinflammatory mediators via upregulation of TLR4 and CD14 in murine microglia
    Bijay Parajuli
    Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Furo cho, Chikusa ku, Nagoya 464 8601, Japan
    J Neuroinflammation 9:268. 2012
    ..GM-CSF has been shown to be associated with neuroinflammatory responses in multiple sclerosis and Alzheimer's disease. However, the mechanisms how GM-CSF promotes neuroinflammation still remain unclear...
  15. pmc Interleukin-34 selectively enhances the neuroprotective effects of microglia to attenuate oligomeric amyloid-β neurotoxicity
    Tetsuya 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...
  16. pmc Interleukin-25 expressed by brain capillary endothelial cells maintains blood-brain barrier function in a protein kinase Cepsilon-dependent manner
    Yoshifumi 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...
  17. pmc The neuroprotective effects of milk fat globule-EGF factor 8 against oligomeric amyloid β toxicity
    Endong 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...
  18. pmc Fingolimod phosphate attenuates oligomeric amyloid β-induced neurotoxicity via increased brain-derived neurotrophic factor expression in neurons
    Yukiko Doi
    Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Furo cho, Chikusa ku, Nagoya, Japan
    PLoS ONE 8:e61988. 2013
    ..These results suggested that the neuroprotective effects of FTY720-P are mediated by upregulated neuronal BDNF levels. Therefore, FTY720-P may be a promising therapeutic agent for neurodegenerative diseases, such as Alzheimer's disease...
  19. doi request reprint Production and functions of IL-33 in the central nervous system
    Satoko 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...
  20. pmc Fractalkine attenuates excito-neurotoxicity via microglial clearance of damaged neurons and antioxidant enzyme heme oxygenase-1 expression
    Mariko 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...
  21. doi request reprint Production and functions of IL-17 in microglia
    Jun 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...
  22. ncbi request reprint Protective effects of nicergoline against neuronal cell death induced by activated microglia and astrocytes
    Tetsuya 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...
  23. ncbi request reprint Autocrine activation of microglia by tumor necrosis factor-alpha
    Reiko 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...
  24. doi request reprint Fingolimod phosphate promotes the neuroprotective effects of microglia
    Hiromi Noda
    Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Furo cho, Chikusa ku, Nagoya 464 8601, Japan
    J Neuroimmunol 256:13-8. 2013
    ..Therefore, FTY720 may be a potent therapeutic agent for not only multiple sclerosis but also other neurologic diseases associated with microglial activation...
  25. doi request reprint TGF-β induced by interleukin-34-stimulated microglia regulates microglial proliferation and attenuates oligomeric amyloid β neurotoxicity
    Di 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...
  26. pmc 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 disease
    Yukiko 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...
  27. doi request reprint Immunoglobulin G(1) immune complex upregulates interferon-γ-induced nitric oxide production via ERK1/2 activation in murine microglia
    Bijay 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...
  28. ncbi request reprint Gene expression profile of spinal motor neurons in sporadic amyotrophic lateral sclerosis
    Yue 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...
  29. doi request reprint Interferon-gamma directly induces neurotoxicity through a neuron specific, calcium-permeable complex of IFN-gamma receptor and AMPA GluR1 receptor
    Tetsuya 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...
  30. ncbi request reprint Chronological changes of CD4(+) and CD8(+) T cell subsets in the experimental autoimmune encephalomyelitis, a mouse model of multiple sclerosis
    Yoshifumi 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...
  31. doi request reprint Microglia express a functional receptor for interleukin-23
    Yoshifumi 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...
  32. ncbi request reprint The radical scavenger edaravone prevents oxidative neurotoxicity induced by peroxynitrite and activated microglia
    Masahiro Banno
    Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Furo cho, Chikusa, Nagoya 464 8601, Japan
    Neuropharmacology 48:283-90. 2005
    ....
  33. doi request reprint Midkine inhibits inducible regulatory T cell differentiation by suppressing the development of tolerogenic dendritic cells
    Yoshifumi 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...
  34. pmc Inhibition of midkine alleviates experimental autoimmune encephalomyelitis through the expansion of regulatory T cell population
    Jinyan 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...
  35. ncbi request reprint Roles of glia-derived cytokines on neuronal degeneration and regeneration
    Akio 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
    ....
  36. ncbi request reprint Production of IL-27 and other IL-12 family cytokines by microglia and their subpopulations
    Yoshifumi 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...
  37. pmc Ablation of keratan sulfate accelerates early phase pathogenesis of ALS
    Kenichi Hirano
    Department of Biochemistry, Nagoya University Graduate School of Medicine, Nagoya, Japan
    PLoS ONE 8:e66969. 2013
    ..This study suggests that KS plays an indispensable, suppressive role in the early phase pathogenesis of ALS and may represent a new target for therapeutic intervention. ..
  38. ncbi request reprint Differential expression of inflammation- and apoptosis-related genes in spinal cords of a mutant SOD1 transgenic mouse model of familial amyotrophic lateral sclerosis
    Tsuyoshi 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...
  39. ncbi request reprint Dorfin prevents cell death by reducing mitochondrial localizing mutant superoxide dismutase 1 in a neuronal cell model of familial amyotrophic lateral sclerosis
    Hideyuki 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...
  40. ncbi request reprint Mitochondrial localization of mutant superoxide dismutase 1 triggers caspase-dependent cell death in a cellular model of familial amyotrophic lateral sclerosis
    Hideyuki 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...
  41. ncbi request reprint Hsp70 and Hsp40 improve neurite outgrowth and suppress intracytoplasmic aggregate formation in cultured neuronal cells expressing mutant SOD1
    Hideyuki 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...
  42. pmc Four-jointed is a Golgi kinase that phosphorylates a subset of cadherin domains
    Hiroyuki 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...