Updated on 2024/07/03

写真a

 
ICHIKI Takako
 
Organization
Academic Assembly Institute of Medicine and Dentistry SHIGAKU KEIRETU Assistant Professor
Faculty of Dentistry Department of Dentistry Assistant Professor
Graduate School of Medical and Dental Sciences Oral Life Science Oral Biological Science Assistant Professor
. Research Associate Professor
Title
Assistant Professor
External link

Degree

  • 医学博士 ( 順天堂大学 )

Research Areas

  • Life Science / Neuroscience-general

  • Life Science / Medical biochemistry

  • Life Science / Physiology

Research History (researchmap)

  • Niigata University   Research Associate Professor

    2023.11

    　 More details

  • Niigata University   Graduate School of Medical and Dental Sciences   Assistant Professor

    2021.5

    　 More details

  • Japan Society for the Promotion of Science

    2020.5 - 2021.4

    　 More details

  • California Institute of Technology   Postdoctoral fellow

    2017.3 - 2021.4

    　 More details

    Country：United States

    researchmap

Research History

  • Niigata University   School of Dentistry, Faculty of Dentistry   Assistant Professor

    2021.5

  • Niigata University   Oral Biological Science, Oral Life Science, Graduate School of Medical and Dental Sciences   Assistant Professor

    2021.5

  • Niigata University   Institute of Medicine and Dentistry, Academic Assembly   Assistant Professor

    2021.5

Professional Memberships

▶ display all

Studying abroad experiences

  • California Institute of Technology  

 

Papers

  • Sensory representation and detection mechanisms of gut osmolality change Reviewed

    Takako Ichiki, Tongtong Wang, Ann Kennedy, Allan-Hermann Pool, Haruka Ebisu, David J. Anderson, Yuki Oka

    Nature   602 ( 7897 )   468 - 474   2022.2

    　More details

    Authorship：Lead author   Publishing type：Research paper (scientific journal)   Publisher：Springer Science and Business Media LLC  

    DOI： 10.1038/s41586-021-04359-5

    researchmap

    Other Link： https://www.nature.com/articles/s41586-021-04359-5

  • Engineered AAVs for non-invasive gene delivery to rodent and non-human primate nervous systems Reviewed

    Xinhong Chen, Sripriya Ravindra Kumar, Cameron D. Adams, Daping Yang, Tongtong Wang, Damien A. Wolfe, Cynthia M. Arokiaraj, Victoria Ngo, Lillian J. Campos, Jessica A. Griffiths, Takako Ichiki, Sarkis K. Mazmanian, Peregrine B. Osborne, Janet R. Keast, Cory T. Miller, Andrew S. Fox, Isaac M. Chiu, Viviana Gradinaru

    Neuron   110 ( 14 )   2242 - 2257.e6   2022.7

    　More details

    Publishing type：Research paper (scientific journal)   Publisher：Elsevier BV  

    DOI： 10.1016/j.neuron.2022.05.003

    researchmap

  • Expression of leukotriene B4 receptor 1 defines functionally distinct DCs that control allergic skin inflammation. Reviewed International journal

    Tomoaki Koga, Fumiyuki Sasaki, Kazuko Saeki, Soken Tsuchiya, Toshiaki Okuno, Mai Ohba, Takako Ichiki, Satoshi Iwamoto, Hirotsugu Uzawa, Keiko Kitajima, Chikara Meno, Eri Nakamura, Norihiro Tada, Yoshinori Fukui, Junichi Kikuta, Masaru Ishii, Yukihiko Sugimoto, Mitsuyoshi Nakao, Takehiko Yokomizo

    Cellular & molecular immunology   18 ( 6 )   1437 - 1449   2021.6

    　More details

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

    Leukotriene B4 (LTB4) receptor 1 (BLT1) is a chemotactic G protein-coupled receptor expressed by leukocytes, such as granulocytes, macrophages, and activated T cells. Although there is growing evidence that BLT1 plays crucial roles in immune responses, its role in dendritic cells remains largely unknown. Here, we identified novel DC subsets defined by the expression of BLT1, namely, BLT1hi and BLT1lo DCs. We also found that BLT1hi and BLT1lo DCs differentially migrated toward LTB4 and CCL21, a lymph node-homing chemoattractant, respectively. By generating LTB4-producing enzyme LTA4H knockout mice and CD11c promoter-driven Cre recombinase-expressing BLT1 conditional knockout (BLT1 cKO) mice, we showed that the migration of BLT1hi DCs exacerbated allergic contact dermatitis. Comprehensive transcriptome analysis revealed that BLT1hi DCs preferentially induced Th1 differentiation by upregulating IL-12p35 expression, whereas BLT1lo DCs accelerated T cell proliferation by producing IL-2. Collectively, the data reveal an unexpected role for BLT1 as a novel DC subset marker and provide novel insights into the role of the LTB4-BLT1 axis in the spatiotemporal regulation of distinct DC subsets.

    DOI： 10.1038/s41423-020-00559-7

    PubMed

    researchmap

  • Neural populations for maintaining body fluid balance Reviewed

    Takako Ichiki, Vineet Augustine, Yuki Oka

    Current Opinion in Neurobiology   57   134 - 140   2019.8

    　More details

    Authorship：Lead author   Publishing type：Research paper (scientific journal)   Publisher：Elsevier BV  

    DOI： 10.1016/j.conb.2019.01.014

    researchmap

  • Stepwise phosphorylation of leukotriene B-4 receptor 1 defines cellular responses to leukotriene B-4 Reviewed International journal

    Nakanishi Yoshimitsu, Tan Modong, Ichiki Takako, Inoue Asuka, Yoshihara Jun-ichi, Maekawa Naoto, Takenoshita Itsuki, Yanagida Keisuke, Yamahira Shinya, Yamaguchi Satoshi, Aoki Junken, Nagamune Teruyuki, Yokomizo Takehiko, Shimizu Takao, Nakamura Motonao

    SCIENCE SIGNALING   11 ( 544 )   2018.8

    　More details

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

    Leukotriene B4 (LTB4) receptor type 1 (BLT1) is abundant in phagocytic and immune cells and plays crucial roles in various inflammatory diseases. BLT1 is phosphorylated at several serine and threonine residues upon stimulation with the inflammatory lipid LTB4 Using Phos-tag gel electrophoresis to separate differentially phosphorylated forms of BLT1, we identified two distinct types of phosphorylation, basal and ligand-induced, in the carboxyl terminus of human BLT1. In the absence of LTB4, the basal phosphorylation sites were modified to various degrees, giving rise to many different phosphorylated forms of BLT1. Different concentrations of LTB4 induced distinct phosphorylation events, and these ligand-induced modifications facilitated additional phosphorylation events at the basal phosphorylation sites. Because neutrophils migrate toward inflammatory sites along a gradient of LTB4, the degree of BLT1 phosphorylation likely increases in parallel with the increase in LTB4 concentration as the cells migrate. At high concentrations of LTB4, deficiencies in these two types of phosphorylation events impaired chemotaxis and β-hexosaminidase release, a proxy for degranulation, in Chinese hamster ovary (CHO-K1) and rat basophilic leukemia (RBL-2H3) cells, respectively. These results suggest that an LTB4 gradient around inflammatory sites enhances BLT1 phosphorylation in a stepwise manner to facilitate the precise migration of phagocytic and immune cells and the initiation of local responses, including degranulation.

    DOI： 10.1126/scisignal.aao5390

    Web of Science

    PubMed

    researchmap

  • Receptor for Advanced Glycation End Products Regulates Leukotriene B4 Receptor 1 Signaling Reviewed

    Takako Ichiki, Tomoaki Koga, Takehiko Yokomizo

    DNA and Cell Biology   35 ( 12 )   747 - 750   2016.12

    　More details

    Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)   Publisher：Mary Ann Liebert Inc.  

    Leukotriene B4 receptor 1 (BLT1), a high-affinity G protein-coupled receptor (GPCR) for leukotriene B4 (LTB4), plays important roles in inflammatory and immune reactions. Although the LTB4-BLT1 axis is known to promote inflammation, the binding proteins that modulate LTB4-BLT1 signaling have not been identified. Recently, we discovered that receptor for advanced glycation end products (RAGE) interacts with BLT1 and modulates LTB4-BLT1 signaling. We propose RAGE as a new class of GPCR modulator and a new target of future GPCR studies.

    DOI： 10.1089/dna.2016.3552

    Scopus

    PubMed

    researchmap

  • Modulation of leukotriene B4 receptor 1 signaling by receptor for advanced glycation end products (RAGE) Reviewed

    Takako Ichiki, Tomoaki Koga, Toshiaki Okuno, Kazuko Saeki, Yasuhiko Yamamoto, Hiroshi Yamamoto, Masakiyo Sakaguchi, Takehiko Yokomizo

    FASEB JOURNAL   30 ( 5 )   1811 - 1822   2016.5

    　More details

    Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)   Publisher：FEDERATION AMER SOC EXP BIOL  

    Leukotriene B-4 (LTB4) receptor 1 (BLT1), a high-affinity GPCR for LTB4, plays important roles in acute and chronic inflammatory diseases. Although the LTB4-BLT1 axis is known to promote inflammation, no studies have defined the binding proteins that modulate LTB4-BLT1 signaling. In this study, the receptor for advanced glycation end products (RAGE) interacted with BLT1 in human cervical epithelial HeLa cells. RAGE increased LTB4-BLT1-dependent ERK phosphorylation and inhibited LTB4-BLT1-dependent activation of NF-kB and up-regulation of proinflammatory cytokines and chemokines. RAGE-dependent inhibition of NF-kB was blunted by treatment with an MEK inhibitor, suggesting that RAGE suppresses LTB4-BLT1-dependent NF-kB signaling by enhancing the MEK-ERK pathway. Meanwhile, in a chemotaxis assay of mouse bone marrow-derived neutrophils, the velocity of LTB4-dependent neutrophil migration was attenuated by soluble RAGE, which is an inhibitory decoy protein for RAGE signaling, in a dose-dependent manner (0.2-5 mg/ml), or by RAGE deficiency. Furthermore, both LTB4-dependent ERK phosphorylation in neutrophils and LTB4-dependent neutrophil accumulation in a murine peritonitis model were significantly attenuated in RAGE-deficient mice compared with C57BL/6J wild-type mice, indicating that RAGE potentiates LTB4-dependent neutrophil migration by enhancing ERK phosphorylation. Our results demonstrate that RAGE interacts with BLT1 and modulates LTB4-BLT1 signaling through potentiation of the MEK-ERK pathway.

    DOI： 10.1096/fj.201500117

    Web of Science

    PubMed

    researchmap

  • Neurokinin B activates the formation and bone resorption activity of rat osteoclasts Reviewed

    Takako Ichiki, Kayoko N. Kuroishi, Kaori K. Gunjigake, Shigeru Kobayashi, Tetsuya Goto

    NEUROPEPTIDES   45 ( 3 )   239 - 244   2011.6

    　More details

    Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)   Publisher：CHURCHILL LIVINGSTONE  

    Neurokinin B (NKB) is a neuropeptide in the tachykinin family that acts as a neurotransmitter and neuromodulator, primarily in the central nervous system. The distribution and role of NKB and its receptor, the neurokinin-3 receptor (NK-3R), in peripheral tissues are poorly understood. In this study, we investigated the distribution of NKB and NK-3R in peripheral tissues as well as the role of NKB in bone metabolism, especially in osteoclast formation and bone resorption activity through NK-3R. The distributions of NKB in intact rat neurons of the trigeminal ganglion (TG) and in axons of periodontal tissue were investigated by immunohistochemistry. Osteoclasts from cultured rat bone marrow cells were used to examine the distribution of NK-3R by immunocytochemistry and RT-PCR and to investigate the effects of NKB on the resorption activity of osteoclasts on ivory slices. We found that NKB immunopositive neurons were localized in the rat TG and that NKB immunopositive axons were distributed in periodontal tissues. Immunoreactivity for NK-3R was found in cultured osteoclasts, and NK-3R mRNA expression in the osteoclasts was confirmed by RT-PCR. The addition of NKB significantly increased the number of osteoclasts and the resorption area compared with the control. These findings suggest that NKB was localized in peripheral neurons and may involve the activation of osteoclast formation and bone resorption through NK-3R. (C) 2011 Elsevier Ltd. All rights reserved.

    DOI： 10.1016/j.npep.2011.03.006

    Web of Science

    PubMed

    researchmap

▶ display all

MISC

  • 神経系による飲水制御～消化管における浸透圧センシング機構～ Invited

    実験医学（増刊）   41 ( 20(増刊) )   3310 - 3316   2023.12

    　More details

    Authorship：Lead author  

    researchmap

  • 消化管における飲水感知メカニズムの解明

    市木貴子, 岡 勇輝

    実験医学   40 ( 9 )   2022.5

    　More details

    Authorship：Lead author  

    DOI： 10.18958/7011-00003-0000168-00

    researchmap

  • 渇きの神経科学：知覚・情報処理・行動の統御

    蛭子はるか, 市木 貴子, 岡 勇輝

    実験医学   36 ( 14 )   2394 - 2399   2018.9

    　More details

    Publishing type：Article, review, commentary, editorial, etc. (trade magazine, newspaper, online media)  

    researchmap

  • 水を感知する味覚受容機構の解明

    Dhruv Zocchi, 市木 貴子, 岡 勇輝

    実験医学   35 ( 16 )   2746 - 2748   2017.10

    　More details

    Authorship：Lead author   Publishing type：Article, review, commentary, editorial, etc. (trade magazine, newspaper, online media)  

    researchmap

  • RAGEはロイコトリエンB4第一受容体BLT1と機能的に相互作用する

    市木 貴子, 古賀 友紹, 奥野 利明, 佐伯 和子, 阪口 政清, 山本 靖彦, 横溝 岳彦

    日本生化学会大会プログラム・講演要旨集   89回   [2P - 089]   2016.9

    　More details

    Language：Japanese   Publisher：(公社)日本生化学会  

    researchmap

  • HMGB1及びLPSに誘導される炎症を抑制する新規低分子化合物の創製

    中島 槙吾, 玉田 賢弥, 佐藤 聡, 吉森 篤史, 市木 貴子, 佐々木 文之, 横溝 岳彦, 田沼 靖一

    日本生化学会大会プログラム・講演要旨集   89回   [2P - 001]   2016.9

    　More details

    Language：Japanese   Publisher：(公社)日本生化学会  

    researchmap

  • HMGB1/RAGE相互作用を阻害する新規低分子化合物の創製

    玉田 賢弥, 中島 槙吾, 佐藤 聡, 吉森 篤史, 市木 貴子, 佐々木 文之, 横溝 岳彦, 鈴木 雄祐, 渡邊 伸央, 井上 茂亮, 田沼 靖一

    日本生化学会大会プログラム・講演要旨集   89回   [1P - 010]   2016.9

    　More details

    Language：Japanese   Publisher：(公社)日本生化学会  

    researchmap

  • Leukotriene receptors

    市木 貴子, 古賀 友紹, 横溝 岳彦

    医学のあゆみ   256 ( 5 )   554 - 560   2016.1

    　More details

    Authorship：Lead author   Language：Japanese   Publisher：医歯薬出版  

    CiNii Article

    CiNii Books

    researchmap

  • P-17 Expression of Neurokinin Receptors in Rat Osteoclasts

    Ichiki Takako, Morikawa Kazumasa, Nakao Kayoko, Gunjigake Kaori, Goto Tetsuya, Kobayashi Shigeru

    The Journal of the Kyushu Dental Society   62 ( 5 )   186 - 187   2009.1

    　More details

    Language：Japanese   Publisher：Kyushu Dental Society  

    CiNii Article

    CiNii Books

    researchmap

▶ display all

Presentations

  • 消化管における飲水制御機構の解明 Invited

    市木 貴子

    第六回 三融会・武田神経科学シンポジウム  2024.5 

    　More details

    Event date： 2024.5

    Presentation type：Oral presentation (invited, special)  

    researchmap

  • 消化管支配神経のin vivo イメージングを用いた飲水感知機構の解明 Invited

    市木 貴子

    第101回日本生理学会大会  2024.3 

    　More details

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

    researchmap

  • 神経系による体液恒常性維持メカニズム Invited

    市木貴子

    第76回日本自律神経学会総会  2023.10 

    　More details

    Presentation type：Oral presentation (invited, special)  

    researchmap

  • Elucidating the sensing mechanisms of gut osmolality change Invited

    Takako Ichiki

    The 46th Annual Meeting of the Japan Neuroscience Society  2023.8 

    　More details

    Presentation type：Symposium, workshop panel (public)  

    researchmap

  • 消化管における飲水感知メカニズムの解明 Invited

    市木貴子

    第70回日本実験動物学会総会  2023.5 

    　More details

    Presentation type：Symposium, workshop panel (nominated)  

    researchmap

  • Representation and sensing mechanisms of gut osmolality in the peripheral sensory ganglia Invited

    Takako Ichiki

    The 100th Anniversary Annual Meeting of The Physiological Society of Japan  2023.3 

    　More details

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

    researchmap

  • 消化管における低浸透圧感知メカニズム Invited

    市木貴子

    第6回感覚フロンティア研究会シンポジウム  2022.10 

    　More details

▶ display all

Awards

  • 令和５年度新年俸制教員特別報奨

    2024.3   新潟大学  

    市木貴子

    　More details

  • 令和５年度新潟大学優秀論文表彰

    2023.10   新潟大学  

    市木貴子

    　More details

  • Della Martin Fellowship in Mental Illness

    2018.6   California Institute of Technology  

    Takako Ichiki

    　More details

  • Best Oral Presentation Award at the 11th Tokyo Respiratory Research Forum

    2014  

    Ichiki Takako

    　More details

  • DENTSPLY Merit Award

    2011  

    Ichiki Takako

    　More details

Research Projects

  • 消化管におけるアレルゲン受容メカニズムの解明

    Grant number：24K02119

    2024.4 - 2028.3

    System name：科学研究費助成事業

    Research category：基盤研究(B)

    Awarding organization：日本学術振興会

    市木 貴子

    　 More details

    Grant amount：\18460000 （ Direct Cost: \14200000 、 Indirect Cost：\4260000 ）

    researchmap

  • 革新的イメージング技術による脳腸相関メカニズムの解明

    Grant number：23829130

    2023.10 - 2027.3

    System name：戦略的創造研究推進事業 さきがけ

    Awarding organization：科学技術振興機構

    　 More details

    Authorship：Principal investigator 

    researchmap

  • The role of hyperpolarization-activated cyclic nucleotide-gated channels in neuropathic pain

    Grant number：23K09350

    2023.4 - 2026.3

    System name：Grants-in-Aid for Scientific Research

    Research category：Grant-in-Aid for Scientific Research (C)

    Awarding organization：Japan Society for the Promotion of Science

    　 More details

    Grant amount：\4810000 （ Direct Cost: \3700000 、 Indirect Cost：\1110000 ）

    researchmap

  • Japan-Denmark joint research projects to identify the novel biological mechanism of anxiety

    Grant number：22KK0140

    2022.10 - 2026.3

    System name：Grants-in-Aid for Scientific Research

    Research category：Fund for the Promotion of Joint International Research (Fostering Joint International Research (B))

    Awarding organization：Japan Society for the Promotion of Science

    　 More details

    Grant amount：\20150000 （ Direct Cost: \15500000 、 Indirect Cost：\4650000 ）

    researchmap

  • 迷走神経による低浸透圧感知メカニズムの解明

    Grant number：22K15223

    2022.4 - 2024.3

    System name：科学研究費助成事業

    Research category：若手研究

    Awarding organization：日本学術振興会

    市木 貴子

    　 More details

    Grant amount：\4680000 （ Direct Cost: \3600000 、 Indirect Cost：\1080000 ）

    researchmap

  • Elucidating the neural mechanisms underlying thirst suppression

    Grant number：21K20685

    2021.8 - 2023.3

    System name：Grants-in-Aid for Scientific Research

    Research category：Grant-in-Aid for Research Activity Start-up

    Awarding organization：Japan Society for the Promotion of Science

    　 More details

    Grant amount：\3120000 （ Direct Cost: \2400000 、 Indirect Cost：\720000 ）

    researchmap

  • Identification of novel mechanism associating psychiatric disorders with periodontitis

    Grant number：21H03109

    2021.4 - 2024.3

    System name：Grants-in-Aid for Scientific Research

    Research category：Grant-in-Aid for Scientific Research (B)

    Awarding organization：Japan Society for the Promotion of Science

    　 More details

    Grant amount：\17550000 （ Direct Cost: \13500000 、 Indirect Cost：\4050000 ）

    researchmap

  • ロイコトリエンＢ４受容体ＢＬＴ１が規定する新規樹状細胞サブセットの機能解析

    Grant number：13J02797

    2013.4 - 2016.3

    System name：科学研究費助成事業

    Research category：特別研究員奨励費

    Awarding organization：日本学術振興会

    市木 貴子

    　 More details

    Grant amount：\3000000 （ Direct Cost: \3000000 ）

    本研究では、生理活性脂質受容体BLT1に対する抗体を用いて樹状細胞サブセットを解析し、BLT1発現量の異なる２つのサブセット(BLT1hi、BLT1lo)の免疫応答における役割を明らかにすることを目的とし、解析を行った。これまでに、この２つのサブセットにTh1細胞分化誘導、T細胞増殖誘導、リンパ節への走化性における役割の違いがあることが明らかになってきたため、Th1応答を制御するのに重要だと考え、in vivo移入実験を行った。セルソーティング後の細胞にDNBSをloadし、それぞれの樹状細胞を感作していないマウスのfootpadに移入し、5日後、耳介にDNFBを塗布し、耳の厚みを24時間毎に測定した。その結果、BLT1hi樹状細胞はBLT1lo樹状細胞に比べて、Th1型の接触性皮膚炎を増悪した。これによりBLT1hi樹状細胞はTh1誘導能の強い樹状細胞であることが示唆された。
    さらに、研究開始時に想定していた研究に加えて、樹状細胞に発現する分子とBLT1の相互作用に興味を持ち、いくつかの分子を対象にBLT1との相互作用を検討した。その結果、RAGEと呼ばれる細胞膜１回貫通型のタンパク質がBLT1と相互作用することを見出した。さらにBLT1とRAGEの相互作用の解析を進めた結果、RAGEがMEK-ERK経路の増強を介してBLT1依存的なサイトカイン産生を抑制し、好中球の走化性を促進することを明らかにした。

    researchmap

▶ display all

 

Teaching Experience (researchmap)

Teaching Experience

  • 生化学実習

    2021
    Institution name：新潟大学