Details of a Researcher - Moriwaki, Yasuhiro

Moriwaki, Yasuhiro

写真a

Affiliation: Faculty of Pharmacy, Department of Pharmacy 薬学教育研究センター（Shiba-Kyoritsu）

Position: Assistant Professor/Senior Assistant Professor

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Career 【 Display / hide 】

2002.04

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2003.03

大阪府立成人病センター研究所, 日本学術振興会特別研究員
2003.04

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2003.08

理化学研究所　脳科学総合研究センター, 日本学術振興会特別研究員
2003.09

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2005.03

理化学研究所　脳科学総合研究センター, 研究員
2005.04

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2007.03

共立薬科大学, 助手
2007.04

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2008.03

共立薬科大学, 助教

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Academic Background 【 Display / hide 】

2000.04

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2003.03

Nara Institute of Science and Technology, Graduate School, Division of Biological Science

Graduate School, Completed, Doctoral course

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Academic Degrees 【 Display / hide 】

博士（バイオサイエンス）, 奈良先端科学技術大学院大学, Coursework, 2003.03

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Licenses and Qualifications 【 Display / hide 】

第一種放射線取扱主任者（選任）, 2022.04

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Papers 【 Display / hide 】

Suppression of Neuroinflammation by Coffee Component Pyrocatechol via Inhibition of NF-κB in Microglia

Murata T, Tago K, Miyata K, Moriwaki Y, Misawa H, Kobata K, Nakazawa Y, Tamura H, Funakoshi-Tago M.

International Journal of Molecular Sciences （International Journal of Molecular Sciences) 25 （ 1 ） 2023.12

Research paper (scientific journal), Joint Work, Accepted
- Access to Document (DOI)
GTS-21 Enhances Regulatory T Cell Development from T Cell Receptor-Activated Human CD4<sup>+</sup> T Cells Exhibiting Varied Levels of CHRNA7 and CHRFAM7A Expression

Mashimo M., Fujii T., Ono S., Moriwaki Y., Misawa H., Azami T., Kasahara T., Kawashima K.

International Journal of Molecular Sciences （International Journal of Molecular Sciences) 24 （ 15 ） 2023.07

Research paper (scientific journal), Accepted, ISSN 16616596

　View Summary

Immune cells such as T cells and macrophages express α7 nicotinic acetylcholine receptors (α7 nAChRs), which contribute to the regulation of immune and inflammatory responses. Earlier findings suggest α7 nAChR activation promotes the development of regulatory T cells (Tregs) in mice. Using human CD4+ T cells, we investigated the mRNA expression of the α7 subunit and the human-specific dupα7 nAChR subunit, which functions as a dominant-negative regulator of ion channel function, under resting conditions and T cell receptor (TCR)-activation. We then explored the effects of the selective α7 nAChR agonist GTS-21 on proliferation of TCR-activated T cells and Treg development. Varied levels of mRNA for both the α7 and dupα7 nAChR subunits were detected in resting human CD4+ T cells. mRNA expression of the α7 nAChR subunit was profoundly suppressed on days 4 and 7 of TCR-activation as compared to day 1, whereas mRNA expression of the dupα7 nAChR subunit remained nearly constant. GTS-21 did not alter CD4+ T cell proliferation but significantly promoted Treg development. These results suggest the potential ex vivo utility of GTS-21 for preparing Tregs for adoptive immunotherapy, even with high expression of the dupα7 subunit.
- Access to Document (DOI)
Regulation of immune functions by non-neuronal acetylcholine (ACh) via muscarinic and nicotinic ACh receptors.

Mashimo M, Moriwaki Y, Misawa H, Kawashima K, Fujii T.

International Journal of Molecular Sciences （MDPI) 22 （ 13 ） 6818 2021.06

Research paper (scientific journal), Joint Work, Accepted, ISSN 16616596

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Acetylcholine (ACh) is the classical neurotransmitter in the cholinergic nervous system. However, ACh is now known to regulate various immune cell functions. In fact, T cells, B cells, and macrophages all express components of the cholinergic system, including ACh, muscarinic, and nicotinic ACh receptors (mAChRs and nAChRs), choline acetyltransferase, acetylcholinesterase, and choline transporters. In this review, we will discuss the actions of ACh in the immune system. We will first briefly describe the mechanisms by which ACh is stored in and released from immune cells. We will then address Ca2+ signaling pathways activated via mAChRs and nAChRs on T cells and B cells, highlighting the importance of ACh for the function of T cells, B cells, and macrophages, as well as its impact on innate and acquired (cellular and humoral) immunity. Lastly, we will discuss the effects of two peptide ligands, secreted lymphocyte antigen-6/urokinase-type plasminogen activator receptor-related peptide-1 (SLURP-1) and hippocampal cholinergic neurostimulating peptide (HCNP), on cholinergic activity in T cells. Overall, we stress the fact that ACh does not function only as a neurotransmitter; it impacts immunity by exerting diverse effects on immune cells via mAChRs and nAChRs.
- Access to Document (DOI)
New pathways for the skin´s stress response: the cholinergic neuropeptide SLURP-1 can activate mast cells and alter cytokine production in mice.

Ertle CM, Rommel FR, Tumala S, Moriwaki Y, Klein J, Kruse J, Gieler U, Peters EMJ.

Frontiers in Immunology （Frontiers in Immunology) 12 631881 2021.03

Research paper (scientific journal), Joint Work, Accepted

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Background: The alpha7 nicotinic acetylcholine receptor (Chrna7) plays an essential anti-inflammatory role in immune homeostasis and was recently found on mast cells (MC). Psychosocial stress can trigger MC hyperactivation and increases pro-inflammatory cytokines in target tissues such as the skin. If the cholinergic system (CS) and Chrna7 ligands play a role in these cascades is largely unknown. Objective: To elucidate the role of the CS in the response to psychosocial stress using a mouse-model for stress-triggered cutaneous inflammatory circuits. Methods: Key CS markers (ACh, Ch, SLURP-1, SLURP-2, Lynx1, Chrm3, Chrna7, Chrna9, ChAT, VAChT, Oct3, AChE, and BChE) in skin and its MC (sMC), MC activation, immune parameters (TNFα, IL1β, IL10, TGFβ, HIF1α, and STAT3) and oxidative stress were analyzed in skin from 24 h noise-stressed mice and in cultured MC (cMC) from C57BL/6 or Chrna7-Knockout mice. Results: First, Chrna7 and SLURP-1 mRNA were exclusively upregulated in stressed skin. Second, histomorphometry located Chrna7 and SLURP-1 in nerves and sMC and demonstrated upregulated contacts and increased Chrna7+ sMC in stressed skin, while 5 ng/mL SLURP-1 degranulated cMC. Third, IL1β+ sMC were high in stressed skin, and while SLURP-1 alone had no significant effect on cMC cytokines, it upregulated IL1β in cMC from Chrna7-KO and in IL1β-treated wildtype cMC. In addition, HIF1α+ sMC were high in stressed skin and Chrna7-agonist AR-R 17779 induced ROS in cMC while SLURP-1 upregulated TNFα and IL1β in cMC when HIF1α was blocked. Conclusions: These data infer that the CS plays a role in the regulation of stress-sensitive inflammatory responses but may have a surprising pro-inflammatory effect in healthy skin, driving IL1β expression if SLURP-1 is involved.
- Access to Document (DOI)
Endogenous neurotoxin-like protein Ly6H inhibits alpha7 nicotinic acetylcholine receptor currents at the plasma membrane.

Moriwaki Y*, Kubo N, Watanabe M, Asano S, Shinoda T, Sugino T, Ichikawa D, Tsuji S, Kato F, Misawa H.

Scientific Reports （Scientific Reports) 10 （ 1 ） 11996 2020.07

Research paper (scientific journal), Joint Work, Lead author, Corresponding author, Accepted

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© 2020, The Author(s). α7 nicotinic acetylcholine receptors (nAChRs) are widely expressed in the central nervous system and regarded as potential therapeutic targets for neurodegenerative conditions, such as Alzheimer’s disease and schizophrenia. Yet, despite the assumed pathophysiological importance of the α7 nAChR, molecular physiological characterization remains poorly advanced because α7 nAChR cannot be properly folded and sorted to the plasma membranes in most mammalian cell lines, thus preventing the analyses in heterologous expression system. Recently, ER-resident membrane protein NACHO was discovered as a strong chaperone for the functional expression of α7 nAChR in non-permissive cells. Ly6H, a brain-enriched GPI-anchored neurotoxin-like protein, was reported as a novel modulator regulating intracellular trafficking of α7 nAChR. In this study, we established cell lines that stably and robustly express surface α7 nAChR by introducing α7 nAChR, Ric-3, and NACHO cDNA into HEK293 cells (Triple α7 nAChR/RIC-3/NACHO cells; TARO cells), and re-evaluated the function of Ly6H. We report here that Ly6H binds with α7 nAChRs on the cell membrane and modulates the channel activity without affecting intracellular trafficking of α7 nAChR.
- Access to Document (DOI)

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Papers, etc., Registered in KOARA 【 Display / hide 】

Development of novel therapeutic strategies for myasthenia gravis.

Moriwaki, Yasuhiro

福澤諭吉記念慶應義塾学事振興基金事業報告集（福澤基金運営委員会) 2021
Development of novel therapeutic strategies for myasthenia gravis

Moriwaki, Yasuhiro

福澤諭吉記念慶應義塾学事振興基金事業報告集（福澤基金運営委員会) 2020
Elucidation of the molecular mechanism of HEG1 in controlling proliferation of mesothelioma cell.

Moriwaki, Yasuhiro

学事振興資金研究成果実績報告書（慶應義塾大学) 2019
A novel therapeutic strategy against psoriasis by using nicotinic acetylcholine receptor modulator, SLURP-1

Moriwaki, Yasuhiro

科学研究費補助金研究成果報告書 2016

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Reviews, Commentaries, etc. 【 Display / hide 】

ニコチン受容体修飾因子SLURP-1による乾癬の新規治療戦略

森脇康博

臨床免疫・アレルギー科 66 ( 1 ) 45 - 49 2016.07

Article, review, commentary, editorial, etc. (trade magazine, newspaper, online media), Single Work
パーキンソン病と小胞体ストレス

森脇康博, 高橋良輔

現代医療 36 ( 4 ) 129 - 134 2004.04

Article, review, commentary, editorial, etc. (trade magazine, newspaper, online media), Joint Work

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Presentations 【 Display / hide 】

腫瘍マーカータンパク質ファミリー、Ly6 super familyの一つであるLy6Hに対するモノクローナル抗体の作製

森脇康博,井上直和, 辻祥太郎.

第43回日本分子腫瘍マーカー研究会,

2023.09
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Oral presentation (general)
Physiological function of Ly6H, a novel endogenous modifier protein of the nicotinic receptor.

森脇康博, 鈴木美帆, 井上直和, 辻祥太郎, 三澤日出巳.

第46回日本神経科学大会,

2023.08
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Poster presentation
内在性神経毒類似タンパク質によるニコチン受容体の機能変換メカニズムの解明

三澤日出巳, 森﨑祐太, 森脇康博.

第37回令和4年度喫煙科学研究財団助成研究発表会,

2023.07
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Oral presentation (general)
コーヒーによる神経炎症の抑制分子メカニズムの解析

村田大典, 森脇康博, 多胡憲治,中澤洋介, 田村悦臣, 多胡めぐみ.

第95回日本生化学会大会 (名古屋) ,

2022.11
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Poster presentation
コーヒー及び含有成分ピロカテコールによる神経炎症の抑制効果

村田大典, 森脇康博, 多胡憲治,中澤洋介, 田村悦臣, 多胡めぐみ.

第66回日本薬学会関東支部大会 (神奈川) ,

2022.09
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Oral presentation (general)

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Research Projects of Competitive Funds, etc. 【 Display / hide 】

次世代抗体医薬品の開発を加速するRI標識に関する基盤技術開発とRI標識抗体医薬の実用化研究

2023.04

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Present

国立研究開発法人日本医療研究開発機構(AMED), 次世代治療・診断実現のための創薬基盤技術開発事業, Coinvestigator(s)
Physiological and pathological roles of functional inhibitors of memory-related nicotinic receptors on memory.

2023.04

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2026.03

基盤研究(C), Principal investigator
重症筋無力症に対する二重特異性抗体薬を用いた根治治療法の開発

2020.04

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2023.03

文部科学省・日本学術振興会, 科学研究費助成事業, 基盤研究(C), Research grant, Principal investigator
新しい糖鎖創薬の標的・HEG1に対する抗体医薬の開発

2018.11

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2021.03

国立研究開発法人日本医療研究開発機構(AMED), 次世代治療・診断実現のための創薬基盤技術開発事業, No Setting
内在性神経毒類似タンパク質によるニコチン受容体調節の生理的役割の解明

2016.04

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2021.03

喫煙科学研究財団, No Setting

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Awards 【 Display / hide 】

第137回日本薬理学会関東部会　若手優秀発表賞

渡邉みずほ, 森脇康博, 久保那月, 加藤総夫, 三澤日出巳., 2017.10, 内在性神経毒素類似タンパク質Ly6Hによるニコチン受容体調整.

Type of Award： Award from Japanese society, conference, symposium, etc.
第131回日本薬理学会関東部会　若手優秀発表賞

森﨑祐太, 坪田充司, 森脇康博, 山中宏二, 三澤日出巳., 2014.10, 筋萎縮性側索硬化症における運動ニューロン変性とオステオポンチン及びマトリックスメタロプロテアーゼ-9の関連の検討.

Type of Award： Award from Japanese society, conference, symposium, etc.