九州大学 研究者情報
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基本情報 研究活動 教育活動 社会活動 病院臨床活動
吉田 晋一郎(よしだ しんいちろう) データ更新日:2020.01.10

助教 /  九州大学病院 口腔機能修復科 九州大学大学院歯学研究院 口腔機能修復学講座 歯科保存学研究分野


主な研究テーマ
新規歯周組織再生療法の開発
キーワード:歯根膜、幹細胞、再生
2012.04.
幹細胞、シグナル因子および足場材を用いた新規歯髄象牙質複合体再生療法の開発
キーワード:歯髄、象牙質、幹細胞、再生
2012.04.
研究業績
主要著書
主要原著論文
1. 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..
2. 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
主要学会発表等
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 日本語雑誌査読論文数 国際会議録査読論文数 国内会議録査読論文数 合計
2019年度      
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)
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.

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