Updated on 2024/07/28

Information

 

写真a

 
MASUDA TAKAHIRO
 
Organization
Medical Institute of Bioregulation Medical Research Center for High Depth Omics Professor
Graduate School of Medical Sciences Department of Medical Sciences(Joint Appointment)
Graduate School of Medical Sciences Department of Medicine(Joint Appointment)
Title
Professor
Contact information
メールアドレス

Degree

  • Ph.D.

Research History

  • 2015.5-2017.5 University of Freiburg (Germany), Visiting Scientist(日本学術振興会・海外特別研究員) 2017.6-2020.2 University of Freiburg (Germany), Postdoc

Research Interests・Research Keywords

  • Research theme:Understanding the nature of CNS macrophages

    Keyword:microglia, CAMs, central nervous system

    Research period: 2020.3

Awards

  • 第20回(令和5年度)日本学術振興会賞

    2023.12   日本学術振興会   脳内マクロファージの統合的理解に向けた多角的研究

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    研究業績「脳内マクロファージの統合的理解に向けた多角的研究」において、第20回日本学術振興会賞受賞者に選ばれた。

  • 2023年度日本神経化学会 優秀賞

    2023.7   日本神経化学会   脳内マクロファージの統合的理解に向けた研究

  • 第1回 石館・上野賞

    2022.11   公益財団法人 中外創薬科学財団   脳内マクロファージの統合的理解と研究基盤の創出

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    受賞者・増田は、脳内マクロファージとして知られるミクログリア細胞および脳境界マクロファージの研究に取り組み、その発生・正常分布メカニズム・多様性・生理機能および病態発症における役割に関する卓越した研究成果を上げてきた(PNAS, 2009; Cell Rep, 2012, 2020; Nature Commun, 2014, 2016; Nature, 2019, 2022; Nature Immunol, 2020; Science 2022など38報)。特に、1細胞解析等の最新技術を駆使した研究では、中枢神経系疾患特異的に出現するヒトミクログリアサブセットを世界で初めて同定した。こうした疾患治療標的の創出に直結する顕著な研究成果が高く評価され、令和3年度 科学技術部門の文部科学大臣表彰若手科学者賞を受賞しました。さらに、当該研究領域のレベルを格段に向上させる汎用性の高い細胞機能操作ツールの独自開発にも成功し、これまでの概念を覆す脳境界マクロファージの発生学的な特徴を明らかにした。今後これらの研究基盤をさらに発展させ、画期的な成果を上げることが期待される。

  • 令和3年度文部科学大臣表彰 若手科学者賞

    2021.4   文部科学省   科学技術に関する研究開発、理解増進等において顕著な成果を収めた者に授与される科学技術分野の文部科学大臣表彰 研究課題:脳内免疫細胞ミクログリアの存在意義解明に向けた包括的研究

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    近年、脳内免疫細胞であるミクログリアが、様々な中枢神経系疾患の発症に関与することが明らかになってきた。そのため、新たな創薬ターゲットとして注目されているが、その存在意義や多様性などの基盤情報、特には ヒトにおける解析データは国際的にみても乏しかった。
    増田隆博 氏は、最先端の網羅的11 細胞解析技術等を駆使して、実験モデル動物のみならず、ヒト脳組織内におけるミクログリアの機能や多様性等に関する包括的な研究を世界に先駆けて取り組んだ。
    本研究成果は、ミクログリアの生命原理の理解に直結する重要な基盤情報であり、ミクログリアの機能的側面および多様性に関する理解を大きく前進させた。今後、ミクログリアを標的とした新規治療薬の創出が加速するものと期待される。

  • 2014年度日本神経化学会奨励賞

    2014.9   日本神経化学会   賞の内容:将来の発展を期待される若手神経化学研究者個人に対して授与する 研究課題:IRF転写因子ファミリーによる活性化ミクログリアの表現型制御

  • Best Poster Prize

    2014.7   Purine2014  

  • Poster of the day (Poster award)

    2012.6   Purine2012  

  • Poster Presentation Award

    2010.10   The 29th Naito Conference- GLIA WORLD- Dynamic function of Glial cells in the Brain  

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    Neuropathic pain occurs after several diseases accompanied by nerve damage, which is characterized by abnormal sensory perception such as tactile allodynia (nocuous response to innocuous mechanical stimuli). This debilitating pain condition arises as a consequence of excessive excitability of neurons in the spinal dorsal horn, and the neuronal hyperexcitability involves signaling from activated spinal microglia that have induced or enhanced expression of various genes including proinflammatory cytokines. However, a key transcription factor regulating gene expression and neuropathic pain states is not identified. Here we report that interferon regulatory factor-8 (IRF-8), a member of IRF family transcription factor, controls gene expression in activated microglia responsible for tactile allodynia. Peripheral nerve injury (PNI) increased the expression of IRF-8 in spinal microglia in a cell type-specific manner. Furthermore, IRF-8-deficient mice (irf8-/-) exhibited a marked reduction in allodynia after PNI compared with wild-type mice without affecting normal pain sensitivity. In contrast, these mice showed a similar pain behavior in an inflammatory chronic pain model. Interestingly, irf8-/- mice failed to increase the expression of genes crucial for producing pain hypersensitivity in the spinal cord following PNI. Together, our present findings suggest that IRF-8 is the crucial intermediary for upregulating pain-related molecules and subsequent neuropathic pain.

  • Best Poster Award

    2009.7  

  • 第82回薬理学会年会優秀発表賞

    2009.3   日本薬理学会   Lyn tyrosine kinase is essential for interferon-γ-dependent spinal microglia activation driving neuropathic painに関する発表

  • Poster Award

    2008.7   The 3rd Asian Pain Symposium  

  • 学会奨励賞

    2007.5   Intrathecal administration of interferon-γ activates spinal microglia and causes long-lasting tactile allodynia という演題での発表で受賞

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Papers

  • Specification of CNS macrophage subsets occurs postnatally in defined niches Reviewed International journal

    Nature   604 ( 7907 )   740 - 748   2022.4

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    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1038/s41586-022-04596-2

  • A spinal microglia population involved in remitting and relapsing neuropathic pain Reviewed International journal

    Kohno K, Shirasaka R, Yoshihara K, Mikuriya S, Tanaka K, Takanami K, Inoue K, Sakamoto H, Ohkawa Y, Masuda T, Tsuda M

    Science   376 ( 6588 )   86 - 90   2022.4

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    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1126/science.abf6805

  • Novel Hexb-based tools for studying microglia in the CNS Reviewed

    Nature Immunology   21 ( 7 )   802 - 815   2020.7

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    Language:Others   Publishing type:Research paper (scientific journal)  

    DOI: 10.1038/s41590-020-0707-4

  • Spatial and temporal heterogeneity of mouse and human microglia at single-cell resolution. Reviewed

    Nature   2019.2

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    Language:Others   Publishing type:Research paper (scientific journal)  

    DOI: 10.1038/s41586-019-0924-x

  • Dorsal horn neurons release extracellular ATP in a VNUT-dependent manner that underlies neuropathic pain. Reviewed

    Masuda T, Ozono Y, Mikuriya S, Kohro Y, Tozaki-Saitoh H, Iwatsuki K, Uneyama H, Ichikawa R, Salter MW, Tsuda M, Inoue K

    Nature communications   7   2016.8

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    Language:Others   Publishing type:Research paper (scientific journal)  

    DOI: 10.1038/ncomms12529

  • Transcription factor IRF5 drives P2X4R+-reactive microglia gating neuropathic pain. Reviewed

    Masuda T, Iwamoto S, Yoshinaga R, Tozaki-Saitoh H, Nishiyama A, Mak TW, Tamura T, Tsuda M, Inoue K

    Nature communications   5   2014.5

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    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1038/ncomms4771

  • Direct neuronal conversion of microglia/macrophages reinstates neurological function after stroke. Reviewed International journal

    #Irie T, #Matsuda T, @Hayashi Y, #Matsuda-Ito K, @Kamiya A, #Masuda T, @Prinz M, #Isobe N, @Kira JI, #Nakashima K

    PNAS   2023.10

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  • A comparative analysis of microglial inducible Cre lines Reviewed International journal

    Travis E Faust, Philip A Feinberg, Ciara O'Connor, Riki Kawaguchi, Andrew Chan, Hayley Strasburger, Maximilian Frosch, Margaret A Boyle, @Takahiro Masuda, Lukas Amann, Klaus-Peter Knobeloch, Marco Prinz, Anne Schaefer, Dorothy P Schafer

    Cell Reports   2023.8

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    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1016/j.celrep.2023.113031

  • Microglial Cytokines Mediate Plasticity Induced by 10 Hz Repetitive Magnetic Stimulation Reviewed International journal

    Eichler A, Kleidonas D, Turi Z, Fliegauf M, Kirsch M, Pfeifer D, @Masuda T, Prinz M, Lenz M, Vlachos A.

    Journal of Neuroscience   2023.4

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    Language:Japanese   Publishing type:Research paper (scientific journal)  

  • Lineage tracing identifies in vitro microglia-to-neuron conversion by NeuroD1 expression Reviewed International journal

    #Irie T, @Matsuda-Ito K, @Matsuda T, @Masuda T, @Prinz M, @Isobe N, @Nakashima K.

    Genes to Cells   2023.3

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    Language:Japanese   Publishing type:Research paper (scientific journal)  

  • CD206+ macrophages transventricularly infiltrate the early embryonic cerebral wall to differentiate into microglia Reviewed International journal

    Hattori Y, Kato D, Murayama F, Koike S, Asai H, Yamasaki A, Naito Y, Kawaguchi A, Konishi H, Prinz M, @Masuda T, Wake H, Miyata T.

    Cell Reports   2023.2

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    Language:Japanese   Publishing type:Research paper (scientific journal)  

  • Mapping the origin and fate of myeloid cells in distinct compartments of the eye by single-cell profiling Invited Reviewed International journal

    Wieghofer P, Hagemeyer N, Sankowski R, Schlecht A, Staszewski O, Amann L, Gruber M, Koch J, Hausmann A, Zhang P, Boneva S, Masuda T, Hilgendorf I, Goldmann T, Boettcher C, Priller J, Rossi FMV, Lange C, Prinz M

    EMBO JOURNAL   40 ( 6 )   2021.3

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    Language:English  

    DOI: 10.15252/embj.2020105123

  • Diet-dependent regulation of TGFβ impairs reparative innate immune responses after demyelination Reviewed International journal

    Bosch-Queralt M, Cantuti-Castelvetri L, Damkou A, Schifferer M, Schlepckow K, Alexopoulos I, Lütjohann D, Klose C, Vaculčiaková L, Masuda T, Prinz M, Monroe KM, Di Paolo G, Lewcock JW, Haass C, Simons M

    2021.2

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  • Profiling peripheral nerve macrophages reveals two macrophage subsets with distinct localization, transcriptome and response to injury Reviewed International journal

    Elke Ydens, Lukas Amann, Bob Asselbergh, Charlotte L Scott, Liesbet Martens, Dorine Sichien, Omar Mossad, Thomas Blank, Sofie De Prijck, Donovan Low, @Takahiro Masuda, Yvan Saeys, Vincent Timmerman, Ralf Stumm, Florent Ginhoux, Marco Prinz, Sophie Janssens , Martin Guilliams

    Nature Neuroscience   2020.5

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    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1038/s41593-020-0618-6

  • Comparative analysis of CreER transgenic mice for the study of brain macrophages: A case study Reviewed International journal

    Louise Chappell-Maor, Masha Kolesnikov, Jung-Seok Kim, Anat Shemer, Zhana Haimon, Jonathan Grozovski, Sigalit Boura-Halfon, @Takahiro Masuda, Marco Prinz, Steffen Jung

    European Journal of Immunology   2020.3

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    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1002/eji.201948342

  • Mapping microglia states in the human brain through the integration of high-dimensional techniques Reviewed

    Nature Neuroscience   2019.12

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    Language:Others   Publishing type:Research paper (scientific journal)  

    DOI: 10.1038/s41593-019-0532-y

  • A Subset of Skin Macrophages Contributes to the Surveillance and Regeneration of Local Nerves Reviewed International journal

    Immunity   2019.6

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    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1016/j.immuni.2019.05.009

  • Macrophage centripetal migration drives spontaneous healing process after spinal cord injury Reviewed International journal

    @Kazu Kobayakawa, @Yasuyuki Ohkawa, @Shingo Yoshizaki, @Tetsuya Tamaru, @Takeyuki Saito, @Ken Kijima, @Kazuya Yokota, @Masamitsu Hara, @Kensuke Kubota, @Yoshihiro Matsumoto, @Katsumi Harimaya, Keiko Ozato, @Takahiro Masuda, @Makoto Tsuda, Tomohiko Tamura, @Kazuhide Inoue, V Reggie Edgerton, Yukihide Iwamoto, @Yasuharu Nakashima, @Seiji Okada

    Science Advances   2019.5

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    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1126/sciadv.aav5086

  • Transcription factor MafB contributes to the activation of spinal microglia underlying neuropathic pain development. Reviewed

    Tozaki-Saitoh H, Masuda J, Kawada R, Kojima C, Yoneda S, Masuda T, Inoue K, Tsuda M

    Glia   67 ( 4 )   729 - 740   2018.11

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    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1002/glia.23570

  • Silencing of TGFβ signalling in microglia results in impaired homeostasis. Reviewed

    Zöller T, Schneider A, Kleimeyer C, Masuda T, Potru PS, Pfeifer D, Blank T, Prinz M, Spittau B

    2018.10

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    Language:Others   Publishing type:Research paper (scientific journal)  

    DOI: 10.1038/s41467-018-06224-y

  • Glucocorticoid regulation of ATP release from spinal astrocytes underlies diurnal exacerbation of neuropathic mechanical allodynia Reviewed

    Takahiro Masuda

    Nature Communications   7   2016.12

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    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1038/ncomms13102

  • A novel P2X4 receptor-selective antagonist produces anti-allodynic effect in a mouse model of herpetic pain. Reviewed

    Matsumura Y, Yamashita T, Sasaki A, Nakata E, Kohno K, Masuda T, Tozaki-Saitoh H, Imai T, Kuraishi Y, Tsuda M, Inoue K

    Scientific reports   6   2016.8

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    Language:Others   Publishing type:Research paper (scientific journal)  

    DOI: 10.1038/srep32461

  • Transcription factor IRF1 is responsible for IRF8-mediated IL-1β expression in reactive microglia. Reviewed

    128 ( 4 )   216 - 220   2015.8

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    Language:Others   Publishing type:Research paper (scientific journal)  

    DOI: 10.1016/j.jphs.2015.08.002

  • Chemokine (C-C motif) receptor 5 is an important pathological regulator in the development and maintenance of neuropathic pain. Reviewed

    Matsushita K, Tozaki-Saitoh H, Kojima C, Masuda T, Tsuda M, Inoue K, Hoka S

    Anesthesiology   120 ( 6 )   1491 - 1503   2014.6

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    Language:Others   Publishing type:Research paper (scientific journal)  

    DOI: 10.1097/aln.0000000000000190

  • IRF8 is a transcriptional determinant for microglial motility. Reviewed

    Masuda T, Nishimoto N, Tomiyama D, Matsuda T, Tozaki-Saitoh H, Tamura T, Kohsaka S, Tsuda M, Inoue K

    Purinergic signalling   10 ( 3 )   515 - 521   2014.5

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    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1007/s11302-014-9413-8

  • IRF8 is a critical transcription factor for transforming microglia into a reactive phenotype. Reviewed

    Masuda T, Tsuda M, Yoshinaga R, Tozaki-Saitoh H, Ozato K, Tamura T, Inoue K

    Cell reports   1 ( 4 )   334 - 340   2012.4

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    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1016/j.celrep.2012.02.014

  • Neuronal CCL21 up-regulates microglia P2X4 expression and initiates neuropathic pain development. Reviewed

    Biber K, Tsuda M, Tozaki-Saitoh H, Tsukamoto K, Toyomitsu E, Masuda T, Boddeke H, Inoue K

    The EMBO journal   30 ( 9 )   1864 - 1873   2011.3

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    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1038/emboj.2011.89

  • IFN-γ receptor signaling mediates spinal microglia activation driving neuropathic pain. Reviewed

    106 ( 19 )   8032 - 8037   2009.4

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    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1073/pnas.0810420106

  • Fibronectin/integrin system is involved in P2X(4) receptor upregulation in the spinal cord and neuropathic pain after nerve injury. Reviewed

    Tsuda M, Toyomitsu E, Komatsu T, Masuda T, Kunifusa E, Nasu-Tada K, Koizumi S, Yamamoto K, Ando J, Inoue K

    Glia   56 ( 5 )   579 - 585   2008.4

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    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1002/glia.20641

  • Lyn tyrosine kinase is required for P2X(4) receptor upregulation and neuropathic pain after peripheral nerve injury. Reviewed

    Tsuda M, Tozaki-Saitoh H, Masuda T, Toyomitsu E, Tezuka T, Yamamoto T, Inoue K

    Glia   56 ( 1 )   50 - 58   2008.1

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    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1002/glia.20591

  • Reduced pain behaviors and extracellular signal-related protein kinase activation in primary sensory neurons by peripheral tissue injury in mice lacking platelet-activating factor receptor Reviewed

    Makoto Tsuda, Satoshi Ishii, Takahiro Masuda, Shigeo Hasegawa, Koji Nakamura, Kenichiro Nagata, Tomohiro Yamashita, Hidemasa Furue, Hidetoshi Tozaki-Saitoh, Megumu Yoshimura, Schuichi Koizumi, Takao Shimizu, Kazuhide Inoue

    JOURNAL OF NEUROCHEMISTRY   102 ( 5 )   1658 - 1668   2007.9

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    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1111/j.1471-4159.2007.04796.x

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Books

  • 実験医学「脳をしなやかに制御するミクログリアと脳内免疫系」 脳実質ミクログリアと脳境界マクロファージ

    @増田隆博( Role: Joint author)

    羊土社  2022.11 

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    Language:Japanese   Book type:Scholarly book

  • 実験医学「脳をしなやかに制御するミクログリアと脳内免疫系」 概論:多様なミクログリアの機能と細胞特性

    @増田隆博( Role: Joint author)

    羊土社  2022.11 

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    Language:Japanese   Book type:Scholarly book

  • 臨床免疫・アレルギー科 特集Ⅱマクロファージの多様性「多様な脳内マクロファージからみる正常脳と中枢神経系疾患」

    @増田隆博( Role: Joint author)

    科学評論社  2022.8 

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    Responsible for pages:第78巻 第2号   Language:Japanese   Book type:Scholarly book

  • 実験医学「神経免疫 メカニズムと疾患 神経系と免疫系を結ぶ分子機構の解明からバイオマーカー・治療標的の探索まで」

    @増田隆博( Role: Joint author)

    羊土社  2021.9 

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    Responsible for pages:Vol.39 No.15, 総論 脳内マクロファージの新時代―多様性が映す中枢性疾患と神経免疫   Language:Japanese   Book type:Scholarly book

  • 実験医学「脳の半分を占める グリア細胞 脳と心と体をつなぐ“膠」

    @増田隆博( Role: Joint author)

    羊土社  2019.10 

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    Responsible for pages:Vol.37 No.17, 単一細胞解析により明らかになったミクログリアの時空間的多様性   Language:Japanese   Book type:Scholarly book

  • 癌と化学療法 Central Nervous System Tumor 脳腫瘍 脳腫瘍と免疫システムUpdate ⅱ脳境界マクロファージと脳免疫システム

    @増田隆博( Role: Joint author)

    癌と化学療法社  2023.6 

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    Language:Japanese   Book type:Scholarly book

  • 炎症と免疫 特集〈Basic Science〉間質リテラシーと疾患:中枢神経系の間質に常在する脳内マクロファージと疾患

    増田隆博( Role: Joint author)

    先端医学社  2023.1 

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    Language:Japanese   Book type:Scholarly book

  • Peripheral Nerve Injury: a Mouse Model of Neuropathic Pain

    @Takahiro Masuda, @Yuta Kohro, @Kazuhide Inoue, @Makoto Tsuda( Role: Joint author)

    Bio-protocol  2017.5 

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    Responsible for pages:Vol 7, Issue 9   Language:English   Book type:Scholarly book

    DOI: https://doi.org/10.21769/BioProtoc.2252

    Other Link: https://bio-protocol.org/e2252

  • 月刊「細胞」 特集「ミクログリアと疼痛」 ミクログリアと神経障害性疼痛

    @増田隆博、@津田誠、@齋藤秀俊、@山下智大、@高露雄太、@井上和秀( Role: Joint author)

    月刊「細胞」  2016.8 

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    Language:Japanese   Book type:Scholarly book

  • Microglia: Lentiviral transduction of cultured microglia

    @Takahiro Masuda, @Makoto Tsuda, @Hidetoshi Tozaki-Saitoh, @Kazuhide Inoue( Role: Joint author)

    2013.8 

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  • Microglia: Intrathecal infusion of microglia cells

    @Takahiro Masuda, @Makoto Tsuda, @Hidetoshi Tozaki-Saitoh, @Kazuhide Inoue( Role: Joint author)

    2013.8 

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Presentations

  • 脳内マクロファージの多様性と中枢神経系疾患

    @増田隆博

    第44回日本炎症・再生医学会  2023.7 

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    Event date: 2024.4

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:大阪   Country:Japan  

  • 脳内マクロファージの分化や機能制御

    @増田隆博

    第35回日本神経免疫学会学術集会  2023.9 

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    Event date: 2024.4

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:東京   Country:Japan  

  • 多様な脳内マクロファージの発生と機能

    @増田隆博

    第96回日本生化学会大会  2023.10 

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    Event date: 2024.4

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Country:Japan  

  • Microglia and CNS border-associated macrophages-similar but different-

    2023.12 

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    Event date: 2024.4

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Country:Japan  

  • Understanding diverse macrophages in the central nervous system

    2023.12 

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    Event date: 2024.4

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Country:Japan  

  • Unraveling the characteristics of macrophages by single-cell analysis

    2023.12 

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    Event date: 2024.4

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Country:Japan  

    Repository Public URL: https://hdl.handle.net/2324/7174513

  • Novel insights into the ontogeny and diversity of CNS macrophages Invited International conference

    @Takahiro Masuda

    The 9th Japan-China Joint Meeting of Basic and Clinical Pharmacology  2023.7 

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    Event date: 2024.4

    Language:English   Presentation type:Symposium, workshop panel (public)  

    Country:China  

  • Diverse macrophages sense and govern brain environment Invited International conference

    @Takahiro Masuda

    16th International Society of Neuroimmunology (ISNI)  2023.8 

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    Event date: 2024.4

    Language:English   Presentation type:Symposium, workshop panel (public)  

    Country:Canada  

  • 脳内免疫系による健やかな脳の形成・維持と破綻 Invited

    @増田隆博

    国立大学附置研究所・センター会議特別シンポジウム  2023.12 

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    Event date: 2024.4

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:東京   Country:Japan  

  • 脳実質と末梢循環系を繋ぐ脳境界領域の形成維持と免疫細胞の特性 Invited

    @増田隆博

    第12回AAA研究会  2024.1 

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    Event date: 2024.4

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:東京   Country:Japan  

  • Diverse macrophages in the central nervous system Invited

    @Takahiro Masuda

    2024.1 

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    Event date: 2024.4

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Country:Japan  

  • シングルセル解析によって明らかになった脳内マクロファージの多様性と細胞特性 Invited

    @増田隆博

    文部科学省認定 共同利用・共同研究拠点 横浜市立大学先端医科学研究センター「マルチオミックスによる遺伝子発現制御の先端的医学共同研究拠点」  2024.2 

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    Event date: 2024.4

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:横浜   Country:Japan  

  • 脳境界マクロファージの発生と維持メカニズム

    @増田隆博

    第129回日本解剖学会総会・全国学術集会  2024.3 

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    Event date: 2024.4

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:沖縄   Country:Japan  

  • Macrophages in the central nervous system: ontogeny and function in health and disease Invited International conference

    2023.2 

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    Event date: 2023.5

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Country:Japan  

  • 脳内マクロファージと脳の発達

    @増田隆博

    第76回日本薬理学会年会  2022.12 

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    Event date: 2023.5

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:横浜   Country:Japan  

  • Diversity of brain macrophages in health and disease Invited International conference

    @Takahiro Masuda

    5th Japan-UK Neuroscience Symposium  2022.9 

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    Event date: 2022.9

    Language:English   Presentation type:Symposium, workshop panel (public)  

    Country:Japan  

  • 多様な脳内マクロファージから紐解く中枢神経系疾患

    @増田隆博

    第43回日本炎症・再生医学会  2022.7 

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    Event date: 2022.7

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:淡路島   Country:Japan  

  • Diverse macrophages govern brain environment

    @Takahiro Masuda

    Neuro2022  2022.8 

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    Event date: 2022.6 - 2022.7

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Country:Japan  

  • Decoding brain environment through single-cell analysis of microglia

    @Takahiro Masuda

    2022.3 

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    Event date: 2022.3

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Country:Japan  

  • 正常時および病態時における中枢神経系マクロファージの多様性

    @増田隆博

    第95回日本薬理学会年会  2022.3 

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    Event date: 2022.3

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:福岡国際会議場   Country:Japan  

  • 脳実質ミクログリアと脳境界マクロファージ Invited

    @増田隆博

    第43回日本疼痛学会  2021.12 

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    Event date: 2022.1

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:オンライン   Country:Japan  

  • マウスおよびヒト脳内におけるミクログリアの多様性および可塑性 Invited

    @増田隆博

    第94回日本生化学会大会  2021.11 

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    Event date: 2022.1

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:オンライン   Country:Japan  

  • Diversity and plasticity of microglia in mice and human Invited

    @Takahiro Masuda

    2021.12 

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    Event date: 2022.1

    Language:English   Presentation type:Symposium, workshop panel (public)  

    Country:Japan  

  • Single-cell analysis reveals spatial and temporal heterogeneity of microglia in human and mice Invited International conference

    @Takahiro Masuda

    2020.9 

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    Event date: 2020.9

    Language:English   Presentation type:Symposium, workshop panel (public)  

    Country:Japan  

  • Microglia heterogeneity and plasticity revealed by single cell analysis Invited

    2019.12 

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    Event date: 2019.12

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Country:Japan  

  • 脳境界免疫細胞を標的とした疾患研究の可能性 Invited

    @増田隆博

    AMED精神・神経疾患領域/早期ライフ連携推進ワークショップ  2023.8 

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    Event date: 2024.4

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Country:Japan  

  • 脳内マクロファージの多様性と機能 Invited

    @増田隆博

    次世代薬理学セミナー2023(日本薬理学会西南部会)  2023.10 

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    Event date: 2024.4

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:オンライン   Country:Japan  

  • Diverse macrophages and brain development Invited International conference

    @Takahiro Masuda

    Young Glia  2023.10 

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    Event date: 2024.4

    Language:English   Presentation type:Oral presentation (general)  

    Country:Japan  

  • Genetic tools for studying diverse macrophages in the CNS International conference

    @Takahiro Masuda

    The 50th Naito Conference  2023.10 

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    Event date: 2024.4

    Language:English   Presentation type:Symposium, workshop panel (public)  

    Country:Japan  

  • Similar but different: Diverse macrophages in the central nervous system Invited International conference

    @Takahiro Masuda

    The 32th Hot Spring Harbor International Symposium  2023.9 

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    Event date: 2024.4

    Language:English   Presentation type:Symposium, workshop panel (public)  

    Country:Japan  

  • 脳内マクロファージの細胞特性や機能を解く Invited

    @増田隆博

    第8回日本骨免疫学会ウィンタースクール  2024.1 

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    Event date: 2024.4

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:長野   Country:Japan  

  • 多様な脳内マクロファージの細胞特性を理解する

    @増田隆博

    第13回日本マーモセット研究会大会  2024.2 

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    Event date: 2024.4

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:東京   Country:Japan  

  • Ontogeny and function of diverse brain macrophages Invited

    @Takahiro Masuda

    International Biomedical Research Seminars  2023.5 

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    Event date: 2023.5

    Language:Japanese   Presentation type:Oral presentation (general)  

    Country:Japan  

  • 多様なマクロファージから脳を知り、制御する Invited

    @増田隆博

    2022.10 

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    Event date: 2023.5

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:オンライン   Country:Japan  

  • 多様な脳内マクロファージから脳の形成と異常を理解する Invited

    @増田隆博

    第16大阪大学ニコンイメージングセンター シリーズセミナー  2023.2 

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    Event date: 2023.5

    Language:Japanese   Presentation type:Oral presentation (invited, special)  

    Venue:大阪   Country:Japan  

  • 多様な脳内マクロファージから見る脳の形成と機能 Invited

    @増田隆博

    第15回 CBIR/ONSA/大学院セミナー共催 若手インスパイアシンポジウム  2023.2 

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    Event date: 2023.5

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:オンライン   Country:Japan  

  • 多様な脳内マクロファージの成り立ちとその後の変化 Invited

    @増田隆博

    令和4年度「感染・免疫・がん・炎症」全国共同研究拠点シンポジウム  2023.3 

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    Event date: 2023.5

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:北海道   Country:Japan  

  • 脳内マクロファージの多様性と中枢神経系疾患

    @増田隆博

    合田パネル第3回創発の場  2023.3 

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    Event date: 2023.5

    Language:Japanese   Presentation type:Oral presentation (general)  

    Country:Japan  

  • 多様な脳内マクロファージから見る脳形成と中枢神経系疾患 Invited

    @増田隆博

    第10回神経と免疫を語る会  2022.7 

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    Event date: 2022.7

    Language:Japanese   Presentation type:Oral presentation (general)  

    Country:Japan  

  • 脳の中に存在する多様なマクロファージを知る Invited

    増田隆博

    第22回NCU Life Science Seminar  2022.8 

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    Event date: 2022.6

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:名古屋市立大学   Country:Japan  

  • 多様な脳内マクロファージと治療標的としての可能性 Invited

    @増田隆博

    第2回SAMURAI研究会  2022.2 

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    Event date: 2022.2

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:オンライン   Country:Japan  

  • IRF family transcription factor axis regulates gene expression program in microglia that gates neuropathic pain

    2012.7 

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    Event date: 2012.7

    Language:Japanese  

    Country:Japan  

  • IRF Family Transcription Factor Axis Governs Gene Expression Program in Microglia Gating Neuropathic Pain International conference

    Takahiro Masuda, Makoto Tsuda, Ryohei Yoshinaga, Nao Nishimoto, Shosuke Iwamoto, Hidetoshi Tozaki-Saitoh, Tomohiko Tamura, Kazuhide Inoue

    Purine2012  2012.6 

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    Event date: 2012.5 - 2012.6

    Language:English   Presentation type:Symposium, workshop panel (public)  

    Country:Japan  

  • IRF family transcription factor axis governs gene expression program in microglia that drives neuropathic pain.

    Takahiro Masuda, Makoto Tsuda, Ryohei Yoshinaga, Nao Nishimoto, Shosuke Iwamoto, Tomohiko Tamura, Kazuhide Inoue

    2012.3 

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    Event date: 2012.3

    Language:English   Presentation type:Oral presentation (general)  

    Country:Japan  

  • 転写因子IRF8を介したミクログリアATP受容体発現制御および神経障害性疼痛における役割

    増田隆博、津田誠、吉永遼平、齊藤秀俊、田村智彦、井上和秀

    プリン研究会  2011.10 

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    Event date: 2011.10

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:岡崎   Country:Japan  

    神経障害などに伴った中枢性疾患発症時、ミクログリアはATP受容体や細胞内シグナル分子を過剰発現させ、炎症性サイトカインなどの生理活性液性因子を過剰産生・放出するなど、劇的にfunctional phenotype shiftを遂げ、「過活動」状態へと移行する。こうした過活動ミクログリアは、神経障害性疼痛発症においても重要な役割を果たしていることは明らかになっているが、ミクログリアの過活動状態への移行を司る遺伝子発現メカニズムは未だ明らかになっていない。本研究で、我々はInterferon regulatory factor-8(IRF8)がミクログリアの過活動状態への移行に重要な役割を果たしていることを見出した。
    末梢神経損傷後、脊髄内でミクログリア特異的にIRF8の顕著な発現増加が観察された。一方、培養ミクログリア細胞にIRF8を強制発現させたところ、P2X4受容体やP2Y12受容体の顕著な発現増加が観察されるなど、過活動状態ミクログリアに見られる特徴的変化を示した。しかし、DNA結合能力の消失した変異型IRF8を遺伝子導入した際には、こうした変化は見られなかった。また、IRF8欠損マウスにおいては、野生型マウスと比較して、末梢神経損傷後に観察されるミクログリア関連分子(P2X4受容体やP2Y12受容体など)の発現増加および疼痛症状が有意に抑制された。以上の結果から、末梢神経損傷後に脊髄ミクログリアで発現増加したIRF8は、ミクログリアの過活動状態への移行に関与し、神経障害性疼痛発症に重要な役割を果たしていると考えられる。

  • Interferon regulatory factor-8 in spinal microglia is a transcription factor crucial for switching to a reactive phenotype after nerve injury

    Takahiro Masuda, Makoto Tsuda, Ryohei Yoshinaga, Hidetoshi Tozaki-Saitoh, Tomohiko Tamura, Kazuhide Inoue

    2011.9 

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    Event date: 2011.9

    Language:English   Presentation type:Oral presentation (general)  

    Country:Japan  

  • IRF8 transcription factor directs microglia to be a hyperactive phenotype driving neuropathic pain International conference

    Takahiro Masuda, Makoto Tsuda, Ryohei Yoshinaga, Hidetoshi Tozaki-Saitoh, Tomohiko Tamura, Kazuhide Inoue

    EuroGlia 2011  2011.9 

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    Event date: 2011.9

    Language:English   Presentation type:Symposium, workshop panel (public)  

    Country:Czech Republic  

  • 転写因子IRF8によるミクログリアの活動性制御および神経障害性疼痛における役割 Invited

    増田隆博、津田誠、吉永遼平、齊藤秀俊、田村智彦、井上和秀

    生理研研究会・グリア細胞機能から迫る脳機能解明  2011.6 

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    Event date: 2011.6

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:岡崎   Country:Japan  

    神経損傷などに伴う中枢性疾患発症時、ミクログリアは細胞機能を司る受容体や細胞内シグナル分子を過剰発現させ、炎症性サイトカインなどの生理活性液性因子を過剰産生・放出するなど、劇的にfunctional phenotype shiftを遂げ、「過活動」状態になる。こうしたミクログリアは、神経障害性疼痛発症においても重要な役割を果たしていることは明らかになっているが、ミクログリアを過活動状態へと移行させる遺伝子発現メカニズムは未だ明らかになっていない。今回、我々はInterferon regulatory factor-8(IRF8)がミクログリアの過活動状態への移行に重要な役割を果たしていることを見出した。
    末梢神経損傷後、脊髄内でミクログリア特異的にIRF8の発現増加が観察された。一方、レンチウィルスベクターを用いて培養ミクログリア細胞にIRF8を強制発現させたところ、機能分子の発現増加など、過活動状態ミクログリアに見られる特徴的変化を示した。しかし、DNA結合能力の消失した変異体IRF8を遺伝子導入した際には、こうした変化は見られなかった。また、IRF8欠損マウスにおいては、野生型マウスと比較して、神経損傷後のミクログリア関連分子の発現増加および疼痛症状が有意に抑制された。以上の結果から、末梢神経損傷後に脊髄ミクログリアで発現増加したIRF8は、ミクログリアの過活動状態への移行に関与し、神経障害性疼痛発症に重要な役割を果たしていると考えられる。

  • IRF8 transcription factor governs gene expression program in microglia that drives neuropathic pain after peripheral nerve injury

    Takahiro Masuda, Makoto Tsuda, Ryohei Yoshinaga, Tomohiko Tamura, Kazuhide Inoue

    2011.3 

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    Event date: 2011.3

    Language:English  

    Country:Japan  

  • 転写因子interferon regulatory factor-8 (IRF8) の神経障害性疼痛における役割

    増田隆博

    第6回九大痛みの研究会  2011.2 

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    Event date: 2011.2

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:福岡   Country:Japan  

  • Interferon regulatory factor-8 in spinal microglia is a transcription factor crucial for the development of neuropathic pain International conference

    Takahiro Masuda, Makoto Tsuda, Ryohei Yoshinaga, Tomohiko Tamura*, Kazuhide Inoue

    GLIA WORLD  2010.10 

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    Event date: 2010.10

    Language:English   Presentation type:Symposium, workshop panel (public)  

    Country:Japan  

  • Interferon regulatory factor-8はミクログリア由来疼痛関連分子の発現を誘導する転写因子である

    2010.9 

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    Event date: 2010.9

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:神戸   Country:Japan  

    Neuropathic pain occurs after several diseases accompanied by nerve damage, which is characterized by abnormal sensory perception such as tactile allodynia (hypersensitivity to innocuous mechanical stimuli). This debilitating pain condition arises as a consequence of excessive excitability of neurons in spinal dorsal horn, and the neuronal hyperexcitability involves signaling from activated spinal microglia that induce or enhance expression of various genes including proinflammatory cytokines. However, a key transcription factor regulating gene expression and neuropathic pain states is not identified. In the present study, we examined the role of interferon regulatory factor-8 (IRF-8), a member of IRF family transcription factor, in regulating tactile allodynia. We found that peripheral nerve injury (PNI) increased the expression of IRF-8 in spinal microglia in a cell type-specific manner. Furthermore, mice lacking IRF-8 (irf8-/-) exhibited a marked reduction in allodynia after PNI compared with wild-type mice without affecting normal pain sensitivity or responses to cold stimuli. In contrast, these mice showed a similar pain behavior in an inflammatory chronic pain model. Interestingly, irf8-/- mice failed to increase the expression of genes crucial for producing pain hypersensitivity in the spinal cord following PNI. Together, our present findings suggest that IRF-8 critically contributes to the pathogenesis of neuropathic pain but not of inflammatory pain.

  • Role of interferon regulatory factor-8 in the pathogenesis of neuropathic pain International conference

    Takahiro Masuda, Makoto Tsuda, Ryohei Yoshinaga, Tomohiko Tamura, Kazuhide Inoue

    Purine 2010  2010.6 

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    Event date: 2010.5 - 2010.6

    Language:English   Presentation type:Oral presentation (general)  

    Country:Spain  

  • 神経障害性疼痛におけるinterferon regulatory factor-8の役割

    第83回日本薬理学会年会  2010.3 

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    Event date: 2010.3

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:大阪   Country:Japan  

    Following peripheral nerve injury (PNI), spinal microglia become activated and are implicated in producing neuropathic pain. Activated microglia induce or enhance expression of various genes (such as proinflammatory cytokines), but a key transcriptional factor in spinal microglia that drives neuropathic pain is not identified. In the present study, we found that PNI increased the expression of interferon regulatory factor-8 (IRF-8), a transcription factor, in the spinal cord microglia. Furthermore, mice lacking IRF-8 exhibited a marked reduction in tactile allodynia (hypersensitivity to innocuous mechanical stimuli) after PNI compared to wild-type littermates without affecting basal pain sensitivity. Interestingly, these mice also failed to increase the expression of crucial factors for producing pain hypersensitivity in the spinal cord. Together, our present findings suggest that IRF-8 critically contributes to the pathogenesis of neuropathic pain after PNI.

  • Interferon-gamma receptor signals are required for spinal microglia activation and neuropathic pain after peripheral nerve injury International conference

    Takahiro Masuda, Makoto Tsuda, Kazuhide Inoue

    Fukuoka Purine 2009  2009.7 

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    Event date: 2009.7

    Language:English   Presentation type:Symposium, workshop panel (public)  

    Country:Japan  

  • Lyn tyrosine kinase is essential for interferon-γ-dependent spinal microglia activation driving neuropathic pain

    第82回日本薬理学会年会  2009.3 

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    Event date: 2009.3

    Language:English   Presentation type:Oral presentation (general)  

    Venue:横浜   Country:Japan  

    After peripheral nerve injury, spinal microglia become activated form, which are critical for producing abnormal pain hypersensitivity, namely allodynia - a hallmark symptom of neuropathic pain. We have previously shown that in normal animals spinal microglia express interferon-γ (IFN-γ) receptors and that stimulating these receptors drive microglia to transform into activated ones and that mice lacking IFN-γ receptor exhibit impaired nerve injury-induced microglia activation and allodynia. However, the detailed mechanisms of IFN-γ-induced microglia activation remain unknown. In this study, we investigated the role of Lyn tyrosine kinase that is implicated in neuropathic pain. We found that intrathecal administration of IFN-γ upregulated the expression of Lyn in spinal microglia. In Lyn-deficient mice (lyn-/-), IFN-γ failed to activate microglia and to generate allodynic behavior. Furthermore, nerve injury-induced activation of microglia in the spinal dorsal horn was markedly suppressed in lyn-/- mice compared to wild-type mice. Together, our findings suggest that IFN-γ produces activation of microglia via Lyn kinase signaling, which in turn leads to allodynia after nerve injury.

  • Interferon-γ and Lyn tyrosine kinase are required for spinal microglia activation and neuropathic pain after peripheral nerve injury International conference

    2008.11 

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    Event date: 2008.11

    Language:English   Presentation type:Symposium, workshop panel (public)  

    Venue:ワシントン   Country:United States  

    Neuropathic pain is a result of peripheral nerve injury in diabetes or cancer. A hallmark of this pain is abnormal sensory perception of pain such as allodynia (hypersensitivity to light stimuli). Spinal microglia exhibiting activated form (proliferation, hypertrophy of their cell bodies) have a crucial role in producing allodynia after nerve injury. We have previously shown that a single intrathecal administration of interferon-γ (IFN-γ) to normal animals produces progressive allodynia and spinal microglia activation and that mice lacking IFN-γ receptor display impaired nerve injury-induced microglia activation and allodynia. However, the detailed mechanisms of IFN-γ-dependent microglia activation remain unknown. In the present study, we examined the role of Lyn tyrosine kinase, upregulated in the spinal cord and involved in generating neuropathic allodynia after nerve injury. We found that intrathecal administration of IFN-γ upregulated the expression of Lyn in spinal microglia. In wild-type (WT) mice, intrathecal IFN-γ injection produced an increase in the number of microglia in the dorsal horn and allodynic behavior. In contrast, these changes were markedly suppressed in Lyn-deficient mice (lyn-/-). Furthermore, nerve injury-induced proliferation of microglia in the ipsilateral dorsal horn in WT mice was also attenuated in lyn-/- mice. Together, our findings suggest that IFN-γ produces the activation of microglia via Lyn kinase signaling, which in turn leads to allodynia after peripheral nerve injury.

  • 末梢神経損傷によるミクログリアの活性化と神経因性疼痛発症におけるIFN-γの役割

    福岡ペイン2008  2008.7 

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    Event date: 2008.7

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:Fukuoka   Country:Japan  

    癌や糖尿病などにより神経が損傷を受けることで、神経因性疼痛が発症する。この疼痛は、非侵害性刺激によって激烈な痛みを感じてしまうアロディニアが特徴的である。近年、我々は神経損傷後に脊髄内で活性化したミクログリアが神経因性疼痛発症に重要な役割を持つことを明らかにしてきた。しかし、これまでにミクログリア活性化の詳細なメカニズムは明らかになっていない。そこで本研究では、神経損傷後に脊髄内で発現増加することが報告されているインターフェロンγ(IFN-γ)に着目し、神経因性疼痛発症およびミクログリア活性化への関与について検討した。
    IFN-γリコンビナントタンパク質を脊髄腔内投与することにより、強力かつ持続的なアロディニア症状を呈した。また、脊髄内でのIFN-γ受容体mRNA発現細胞はミクログリアのみであったことから、IFN-γ処置動物の脊髄におけるミクログリアを免疫染色法で観察した。その結果、ミクログリアは異常な活性化(増殖・細胞体の肥大化)を起こしていることが明らかになった。
    続いて、IFN-γ受容体欠損マウスと用いて検討を行ったところ、野生型マウスに比べ、神経損傷後のアロディニア症状および損傷側脊髄後角でのミクログリア活性化に劇的な改善が観察された。
    以上のことより、末梢神経損傷により脊髄内で発現増加するIFN-γは直接ミクログリアに作用し、その活性化を介して神経因性疼痛発症に重要な役割を持つことが明らかになった。

  • Role of interferon-γ in spinal microglia activation and neuropathic pain after peripheral nerve injury International conference

    2008.7 

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    Event date: 2008.7

    Language:English  

    Venue:Fukuoka   Country:Japan  

    Neuropathic pain is a result of peripheral nerve injury in diabetes or cancer. A hallmark of this pain is abnormal sensory perception of pain such as allodynia (hypersensitivity to light stimuli). We have previously shown that spinal microglia exhibiting activated form have a crucial role in producing allodynia after nerve injury. However, the mechanisms of microglia activation remain unknown. In the present study, we examined the role of interferon-γ (IFN-γ), reported to be upregulated in the spinal cord of animal models of neuropathic pain, in microglial activation and neuropathic allodynia. We found that intrathecal administration of IFN-γ produced long-lasting allodynia. The expression of IFN-γ receptor mRNA in the spinal cord of naïve rats was present only in microglia. In the dorsal horn of IFN-γ-treated rats, microglia dramatically changed their morphology into hypertrophy and also proliferated, both of which are prominent features of activated microglia. We next examined the role of IFN-γ in tactile allodynia and microglia activation after peripheral nerve injury using mice lacking IFN-γ receptor (ifngr-/-). We found that ifngr-/- mice exhibited a marked reduction in tactile allodynia after nerve injury compared with wild-type (WT) mice. Furthermore, in WT mice, nerve injury increased the number of microglial cells with hypertrophic morphology in the ipsilateral dorsal horn. In contrast, these changes were markedly suppressed in ifngr-/- mice. Together, our present findings suggest that the IFN-γ/IFN-γ receptor system has crucial roles in activating microglia and producing tactile allodynia after nerve injury.

  • Interferon-γ signals were required in spinal microglia activation and neuropathic pain after peripheral nerve injury International conference

    2008.7 

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    Event date: 2008.6 - 2008.7

    Language:English   Presentation type:Symposium, workshop panel (public)  

    Venue:コペンハーゲン   Country:Denmark  

    Neuropathic pain is a result of peripheral nerve injury in diabetes or cancer. A hallmark of this pain is abnormal sensory perception of pain such as allodynia (hypersensitivity to light stimuli). We have previously shown that spinal microglia exhibiting activated form have a crucial role in producing allodynia after nerve injury. However, the mechanisms of microglia activation remain unknown. In the present study, we examined the role of interferon-γ (IFN-γ), reported to be upregulated in the spinal cord of animal models of neuropathic pain, in microglial activation and neuropathic allodynia. We found that intrathecal administration of IFN-γ produced long-lasting allodynia. The expression of IFN-γ receptor mRNA in the spinal cord of naïve rats was present only in microglia. In the dorsal horn of IFN-γ-treated rats, microglia dramatically changed their morphology into hypertrophy and also proliferated, both of which are prominent features of activated microglia. We next examined the role of IFN-γ in tactile allodynia and microglia activation after peripheral nerve injury using mice lacking IFN-γ receptor (ifngr-/-). We found that a strong allodynia and microglia activation in spinal dorsal horn were markedly attenuated in ifngr-/- mice compared with wild-type (WT) mice. We also found that P2X4 receptor deficient mice failed to exhibit allodynic behavior as observed in WT mice after intrathecal IFN-γ administration. Together, our present findings suggest that the IFN-γ/IFN-γ receptor system has crucial roles in activating microglia, and producing tactile allodynia presumably via P2X4 receptor after nerve injury.

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MISC

  • Lipid in microglial biology - from material to mediator. Reviewed

    @Yamamoto S, @Masuda T

    Inflammation and Regeneration   2023.7

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    Language:English   Publishing type:Article, review, commentary, editorial, etc. (scientific journal)  

    DOI: 10.1186/s41232-023-00289-z

  • Mechanisms of myeloid cell entry to the healthy and diseased central nervous system Reviewed

    Amann L, Masuda T, Prinz M

    Nature Immunology   2023.3

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    Language:Japanese   Publishing type:Article, review, commentary, editorial, etc. (scientific journal)  

  • Novel insights into the origin and development of CNS macrophage subsets Reviewed

    @Masuda T, Amann L, Prinz M

    Clin Transl Med   2022.11

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  • Microglia states and nomenclature: A field at its crossroads Reviewed

    Neuron   2022.11

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    Language:English   Publishing type:Article, review, commentary, editorial, etc. (scientific journal)  

    DOI: 10.1016/j.neuron.2022.10.020.

  • Microglia and Central Nervous System-Associated Macrophages-From Origin to Disease Modulation Reviewed

    Prinz M, @Masuda T, Wheeler MA, Quintana FJ

    Annual Review of Immunology   2021.4

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    DOI: 10.1146/annurev-immunol-093019-110159

  • Microglia Heterogeneity in the Single-Cell Era Reviewed

    @Masuda T, Sankowski R, Staszewski O, Prinz M

    Cell Reports   2020.2

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    DOI: doi: 10.1016/j.celrep.2020.01.010.

  • Macrophages at CNS interfaces: ontogeny and function in health and disease Reviewed

    Kierdorf K, @Masuda T, Jordao M, Prinz M

    Nature Reviews Neuroscience   2019.9

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    DOI: DOI: 10.1038/s41583-019-0201-x

  • Microglial diversity in neuropathic pain Reviewed

    Tsuda M, Masuda T, Kohno K

    Trends in Neuroscience   2023.5

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  • Recent topics regarding macrophage in the central nervous system Reviewed

    @Masuda T

    Journal of Biochemistry   2022.11

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  • 脳内免疫細胞ミクログリアの時空間的多様性 Reviewed

    @増田隆博

    神経化学トピックス   2019.6

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    DOI: DOI: 10.11481/topics107

  • Transcriptional regulation in microglia and neuropathic pain Reviewed

    @Masuda T, @Tsuda M, @Inoue K

    Pain Management   2016.4

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  • Microglia: A Unique Versatile Cell in the Central Nervous System Reviewed

    @Masuda T, Prinz M

    ACS Chemical Neuroscience   2016.4

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    Language:English   Publishing type:Article, review, commentary, editorial, etc. (scientific journal)  

    DOI: DOI: 10.1021/acschemneuro.5b00317

  • P2X4 receptors and neuropathic pain

    Makoto Tsuda, Takahiro Masuda, Hidetoshi Tozaki-Saitoh, Kazuhide Inoue

    Front Cell Neurosci.   2013.10

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  • Microglial regulation of neuropathic pain

    Makoto Tsuda, Takahiro Masuda, Hidetoshi Tozaki-Saitoh, Kazuhide Inoue

    Journal of Pharmacological Sciences   2013.1

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Professional Memberships

  • The Japanese Pharmacological Society

  • The Japanese Society of Neurochemistry

  • Japanese Association for Study of Pain

  • Japanese Society for Immunology

  • The Japanese Neuroscience Society

  • The Japanese Society of Inflammation and regeneration

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Academic Activities

  • Screening of academic papers

    Role(s): Peer review

    2023

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    Type:Peer review 

    Number of peer-reviewed articles in foreign language journals:13

    Number of peer-reviewed articles in Japanese journals:0

    Proceedings of International Conference Number of peer-reviewed papers:0

    Proceedings of domestic conference Number of peer-reviewed papers:0

  • Screening of academic papers

    Role(s): Peer review

    2022

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    Type:Peer review 

    Number of peer-reviewed articles in foreign language journals:13

    Number of peer-reviewed articles in Japanese journals:0

    Proceedings of International Conference Number of peer-reviewed papers:0

    Proceedings of domestic conference Number of peer-reviewed papers:0

  • Screening of academic papers

    Role(s): Peer review

    2021

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    Type:Peer review 

    Number of peer-reviewed articles in foreign language journals:11

    Number of peer-reviewed articles in Japanese journals:0

    Proceedings of International Conference Number of peer-reviewed papers:0

    Proceedings of domestic conference Number of peer-reviewed papers:0

  • Frontiers in Cellular Neuroscience International contribution

    2020.9 - 2021.6

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    Type:Academic society, research group, etc. 

  • Screening of academic papers

    Role(s): Peer review

    2020

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    Type:Peer review 

    Number of peer-reviewed articles in foreign language journals:16

    Number of peer-reviewed articles in Japanese journals:0

    Proceedings of International Conference Number of peer-reviewed papers:0

    Proceedings of domestic conference Number of peer-reviewed papers:0

Research Projects

  • 令和6年度日本人独立研究者始動助成金/脳境界構成細胞を標的とした新規疾患制御ストラテジーの探索

    2024

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    Grant type:Donation

  • 2023年度研究助成金/脳境界領域を取り巻く細胞群による脳機能制御メカニズムの解明と機能的介入法の確立

    2024

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    Grant type:Donation

  • 脳内マクロファージの多様性と中枢神経系疾患

    2023 - 2030

    創発的研究支援事業

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    Authorship:Principal investigator  Grant type:Contract research

  • グリア細胞の生理機構解明とその遷移による中枢神経疾患に対する創薬戦略の国際共同開発

    2023 - 2028

    AMED 医療分野国際科学技術共同研究開発推進事業(先端国際共同研究推進プログラムASPIRE)

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    Authorship:Coinvestigator(s)  Grant type:Contract research

  • 非神経細胞のストレスエングラムから読み解く心的フレイルの統合的理解と診断的治療への応用

    2023 - 2028

    革新的先端研究開発支援事業(AMED-CREST)

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    Authorship:Principal investigator  Grant type:Contract research

  • Elucidation of Mechanisms of the Centenarian Dynamic Resilience through Immune Systems

    2023 - 2027

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    Authorship:Coinvestigator(s)  Grant type:Contract research

  • 2023年度 ビジョナリーリサーチ継続助成(ホップ)/脳内マクロファージサブタイプの機能分離解析に基づく中枢神経系疾患発症メカニズムの理解と新規治療法の創出

    2023

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    Grant type:Donation

  • PIセットアップ研究助成/脳内マクロファージを切り口とした中枢神経系疾患発症メカニズムの理解

    2023

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    Grant type:Donation

  • 2023 年度助成金/中枢性疾患に関わる脳内マクロファージの統合的理解

    2023

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    Grant type:Donation

  • 2023年度持田記念研究助成金/脳境界免疫を基軸とした中枢性疾患発症メカニズムの理解

    2023

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    Grant type:Donation

  • 2023年度 研究助成⾦/脳境界マクロファージによる疾患制御メカニズムの解明

    2023

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    Grant type:Donation

  • 2023年度研究助成金/脳境界構成細胞を標的とした疾患発症メカニズムの統合的理解

    2023

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    Grant type:Donation

  • 神経系疾患発症に紐づく間質性細胞間クロストークの包括的理解

    Grant number:22H05062  2022 - 2024

    日本学術振興会・文部科学省  科学研究費助成事業  学術変革領域研究(B)

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    Authorship:Principal investigator  Grant type:Scientific research funding

  • 新規細胞機能操作ツールを用いた中枢性疾患発症メカニズムの理解

    Grant number:21H02752  2021 - 2024

    日本学術振興会  科学研究費助成事業  基盤研究(B)

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    Authorship:Principal investigator  Grant type:Scientific research funding

  • 慢性ストレス・老化による脳機能変容の炎症性機序の解明

    2021 - 2024

    AMED 脳とこころの研究推進プログラム(精神・神経疾患メカニズム解明プロジェクト)

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    Authorship:Coinvestigator(s)  Grant type:Contract research

  • 精神疾患発症における脳内免疫細胞CAMsの可能性

    Grant number:21H00204  2021 - 2022

    日本学術振興会・文部科学省  科学研究費助成事業  新学術領域研究(研究領域提案型)

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    Authorship:Principal investigator  Grant type:Scientific research funding

  • 稲盛研究助成/脳境界マクロファージの包括的解析から見る正常脳形成と中枢性疾患発症

    2021

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    Grant type:Donation

  • 武田科学振興財団 ビジョナリーリサーチ助成(スタート)/ 脳内マクロファージサブタイプの機能分離解析に基づく中枢神経系疾患発症メカニズムの理解と新規治療法の創出

    2021

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    Grant type:Donation

  • 早期ライフステージの脳内免疫細胞から紐解く正常脳形成と中枢性疾患発症

    2020 - 2023

    革新的先端研究開発支援事業(AMED-PRIME)

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    Authorship:Principal investigator  Grant type:Contract research

  • 中枢神経系マクロファージの機能解明を目的とした新規研究基盤の創出

    Grant number:20K22687  2020 - 2021

    日本学術振興会  科学研究費助成事業  研究活動スタート支援

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    Authorship:Principal investigator  Grant type:Scientific research funding

  • 内藤記念科学奨励金 研究助成/ 新規機能操作ツールを用いた各種脳内マクロファージの存在意義の理解

    2020

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    Grant type:Donation

  • 研究助成金/ 脳内マクロファージの機能解明に向けた基盤情報および新規ツールの創出

    2020

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    Grant type:Donation

  • ミクログリア前駆細胞の脳内定着メカニズムの解明

    2015 - 2017

    日本学術振興会  海外特別研究員

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    Authorship:Principal investigator  Grant type:Joint research

  • 海外留学助成金/中枢神経系組織におけるミクログリア細胞の不均一性

    2015

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    Grant type:Donation

  • IRFとターゲットとしたミクログリアによる神経障害性疼痛発現メカニズムの解明

    Grant number:23890148  2011 - 2012

    科学研究費助成事業  若手研究(スタートアップ)

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    Authorship:Principal investigator  Grant type:Scientific research funding

  • 神​経​因​性​疼​痛​に​お​け​る​I​F​N​-​γ​を​介​し​た​ミ​ク​ロ​グ​リ​ア​の​活​性​化​機​構

    Grant number:20・5285  2008 - 2010

    日本学術振興会  科学研究費助成事業  特別研究員奨励費

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    Authorship:Principal investigator  Grant type:Scientific research funding

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Class subject

  • 医学研究特論Ⅰ

    2023.4 - 2024.3   Full year

  • アカデミック・フロンティアⅠ

    2023.4 - 2023.6   Spring quarter

  • 薬理・基礎理論

    2022.10 - 2023.3   Second semester

  • 基幹教育セミナー

    2022.6 - 2022.8   Summer quarter

FD Participation

  • 2024.4   Role:Participation   Title:職場における落とし穴

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2022.4   Role:Participation   Title:学生の多様性に対応した教育とは:障害学生への合理的配慮を中心に

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2021.9   Role:Participation   Title:JST 次世代研究者挑戦的研究プログラム 説明会

    Organizer:University-wide

  • 2021.9   Role:Participation   Title:M2B学習支援システム講習会★初級・中上級編★

    Organizer:University-wide

  • 2021.7   Role:Participation   Title:生体防御医学研究所FD

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2021.4   Role:Participation   Title:令和3年度 第1回全学FD(新任教員の研修)

    Organizer:University-wide

  • 2021.2   Role:Participation   Title:創薬産学官連携セミナー

    Organizer:[Undergraduate school/graduate school/graduate faculty]

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Other educational activity and Special note

  • 2022  Class Teacher