九州大学-研究者情報 [吉田晋一郎 (助教) 九州大学病院口腔機能修復科]

1.	Yoshida S, Sugii H, Itoyama T, Kadowaki M, Hasegawa D, Tomokiyo A, Hamano S, Ipposhi K, Yamahita K, Maeda H., Development of a novel direct pulp-capping material using 4-META/MA-TBB resin with nanohydroxyapatite., Materials Science and Engineering: C, 10.1016/j.msec.2021.112426, 2021.11.
2.	吉田晋一郎，和田尚久，長谷川大学，御手洗裕美，有馬麻衣，友清淳，濱野さゆり，杉井英樹，前田英史., 骨組織上に播種した歯髄幹細胞は歯根膜関連遺伝子を発現する., 日本歯科保存学会誌, 2018.12.
3.	Shinichiro Yoshida, Naohide Yamamoto, Naohisa Wada, Atsushi Tomokiyo, Daigaku Hasegawa, Sayuri Hamano, Hiromi Mitarai, Satoshi Monnouchi, Asuka Yuda, Hidefumi Maeda, GDNF from Human Periodontal Ligament Cells Treated with Proinflammatory Cytokines Promotes Neurocytic Differentiation of PC12 Cells., Journal of Cellular Biochemistry, 2016.07, Glial cell line-derived neurotrophic factor (GDNF) is known to mediate multiple biological activities such as promotion of cell motility and proliferation, and morphogenesis. However, little is known about its effects on periodontal ligament (PDL) cells. Recently, we reported that GDNF expression is increased in wounded rat PDL tissue and human PDL cells (HPDLCs) treated with proinflammatory cytokines. Here, we investigated the associated expression of GDNF and the proinflammatory cytokine interleukin-1 beta (IL-1β) in wounded PDL tissue, and whether HPDLCs secrete GDNF which affects neurocytic differentiation. Rat PDL cells near the wounded area showed intense immunoreactions against an anti-GDNF antibody, where immunoreactivity was also increased against an anti-IL-1β antibody. Compared with untreated cells, HPDLCs treated with IL-1β or tumor necrosis factor-alpha showed an increase in the secretion of GDNF protein. Conditioned medium of IL-1β-treated HPDLCs (IL-1β-CM) increased neurite outgrowth of PC12 rat adrenal pheochromocytoma cells. The expression levels of two neural regeneration-associated genes, growth-associated protein-43 (Gap-43) and small proline-rich repeat protein 1A (Sprr1A), were also upregulated in IL-1β-CM-treated PC12 cells. These stimulatory effects of IL-1β-CM were significantly inhibited by a neutralizing antibody against GDNF. In addition, U0126, a MEK inhibitor, inhibited GDNF-induced neurite outgrowth of PC12 cells. These findings suggest that an increase of GDNF in wounded PDL tissue might play an important role in neural regeneration probably via the MEK/ERK signaling pathway..
4.	Shinichiro Yoshida, Naohisa Wada, Daigaku Hasegawa, Hirofumi Miyaji, Hiromi Mitarai, Atsushi Tomokiyo, Sayuri Hamano, Hidefumi Maeda, Semaphorin 3A Induces Odontoblastic Phenotype in Dental Pulp Stem Cells, Journal of Dental Research, 2016.06, In cases of pulp exposure due to deep dental caries or severe traumatic injuries, existing pulp-capping materials have a limited ability to reconstruct dentin-pulp complexes and can result in pulpectomy because of their low potentials to accelerate dental pulp cell activities, such as migration, proliferation, and differentiation. Therefore, the development of more effective therapeutic agents has been anticipated for direct pulp capping. Dental pulp tissues are enriched with dental pulp stem cells (DPSCs). Here, the authors investigated the effects of semaphorin 3A (Sema3A) on various functions of human DPSCs in vitro and reparative dentin formation in vivo in a rat dental pulp exposure model. Immunofluorescence staining revealed expression of Sema3A and its receptor Nrp1 (neuropilin 1) in rat dental pulp tissue and human DPSC clones. Sema3A induced cell migration, chemotaxis, proliferation, and odontoblastic differentiation of DPSC clones. In addition, Sema3A treatment of DPSC clones increased β-catenin nuclear accumulation, upregulated expression of the FARP2 gene (FERM, RhoGEF, and pleckstrin domain protein 2), and activated Rac1 in DPSC clones. Furthermore, in the rat dental pulp exposure model, Sema3A promoted reparative dentin formation with dentin tubules and a well-aligned odontoblast-like cell layer at the dental pulp exposure site and with novel reparative dentin almost completely covering pulp tissue at 4 wk after direct pulp capping. These findings suggest that Sema3A could play an important role in dentin regeneration via canonical Wnt/β-catenin signaling. Sema3A might be an alternative agent for direct pulp capping, which requires further study..

主要総説, 論評, 解説, 書評, 報告書等

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Shinichiro Yoshida, Atsushi Tomokiyo, Daigaku Hasegawa, Sayuri Hamano, Hideki Sugii, Hidefumi Maeda., Insight into the Role of Dental pulp Stem Cells in Regenerative Therapy, Biology, 2020.07, Mesenchymal stem cells (MSCs) have the capacity for self-renewal and multilineage differentiation potential, and are considered a promising cell population for cell-based therapy and tissue regeneration. MSCs are isolated from various organs including dental pulp, which originates from cranial neural crest-derived ectomesenchyme. Recently, dental pulp stem cells (DPSCs) and stem cells from human exfoliated deciduous teeth (SHEDs) have been isolated from dental pulp tissue of adult permanent teeth and deciduous teeth, respectively. Because of their MSC-like characteristics such as high growth capacity, multipotency, expression of MSC-related markers, and immunomodulatory effects, they are suggested to be an important cell source for tissue regeneration. Here, we review the features of these cells, their potential to regenerate damaged tissues, and the recently acquired understanding of their potential for clinical application in regenerative medicine..

吉田晋一郎、前田英史, 4-META/MMA-TBBレジンの直接覆髄材への応用, 日本歯内療法学会雑誌, 2019.05.

主要学会発表等

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学会活動

所属学会名

日本再生医療学会

International Association for Dental Research

日本歯内療法学会

日本歯科保存学会

学術論文等の審査

年度	外国語雑誌査読論文数	合計
2021年度	1	1
2020年度	2	2
2019年度	3	3
2018年度	1	1

その他の研究活動

海外渡航状況, 海外での教育研究歴

ADA Forsyth Institute, UnitedStatesofAmerica, 2022.04～2024.03.

外国人研究者等の受入れ状況

2024.04, China.

2022.04, China.

2019.04～2024.03, Syria.

2018.04, Syria.

受賞

JEA理事長賞, 日本歯内療法学会, 2018.06.

JEAワカイ賞, 日本歯内療法学会, 2018.06.

ジーシー優秀ポスター賞, 日本歯科保存学会, 2018.06.

日本歯科保存学会奨励賞, 日本歯科保存学会, 2017.06.

日本歯科保存学会学会賞, 日本歯科保存学会, 2016.10.

JEA会長賞, 日本歯内療法学会, 2016.07.

研究資金

科学研究費補助金の採択状況(文部科学省、日本学術振興会)

2021年度～2023年度, 基盤研究(C), 転写因子PAX9を標的とした歯根膜幹細胞誘導因子の同定.

2021年度～2023年度, 挑戦的研究（萌芽）, 神経堤細胞賦活化低分子化合物を核とする次世代型歯周組織再生薬の創出.

2020年度～2022年度, 若手研究, 代表, ナノハイドロキシアパタイト含有レジンを用いた新規接着性直接覆髄材の創製.

2018年度～2020年度, 挑戦的萌芽研究, 分担, iPS創薬とゲノム創薬の融合による歯根膜細胞賦活化物質の創出と再生医療への応用.

2017年度～2020年度, 基盤研究(B), 分担, iPS由来神経堤細胞によるバイオミメティクスに基づいた新規歯周組織再生療法の開発.

2017年度～2021年度, 基盤研究(A), 分担, iPS細胞を用いた3次元的歯根膜作製法の確立と人工歯根開発への応用.

2017年度～2018年度, 若手研究(B), 代表, 広範囲の欠損修復を可能とする生体親和性良好な新規直接覆髄剤料の開発.

2016年度～2017年度, 研究活動スタート支援, 代表, Semaphorin 3A を用いた新規直接覆髄剤の開発.

学内資金・基金等への採択状況

2019年度～2020年度, QRプログラムわかばチャレンジ, 歯牙の長期維持を可能とする生体親和性良好な新規直接覆髄材の開発.

九大関連コンテンツ

pure2017年10月2日から、「九州大学研究者情報」を補完するデータベースとして、Elsevier社の「Pure」による研究業績の公開を開始しました。

QIR　九州大学学術情報リポジトリシステム情報科学研究院

九州大学病院


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