Updated on 2024/10/09

Information

 

写真a

 
SONODA SOICHIRO
 
Organization
Faculty of Dental Science Department of Dental Science Assistant Professor
School of Dentistry Department of Dentistry（Concurrent）
Graduate School of Dental Science （Concurrent）
Graduate School of Dental Science Department of Dental Science（Concurrent）
Title
Assistant Professor
Contact information
メールアドレス
Tel
0926426302
Profile
1. 再生医療におけるヒト間葉系幹細胞を応用したトランスレーショナルリサーチ 2. 間葉系幹細胞の起源と特性、動態の解析 3. 歯学部生を対象とした解剖学実習、歯牙解剖実習 4. 学部学生および大学院生の研究指導
External link

Degree

  • PhD

Research Interests・Research Keywords

  • Research theme：Dental-pulp/Oral tissue-derived stem cell research

    Keyword：Stem cell, Regenerative medicine, Etiology analysis, Translational research

    Research period： 2018.6

Awards

  • 日本歯科保存学会奨励賞

    2017.6   日本歯科保存学会  

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    Soichiro Sonoda, Haruyoshi Yamaza, Lan Ma, Yosuke Tanaka, Erika Tomoda, Reona Aijima, Kazuaki Nonaka, Toshio Kukita, Songtao Shi, Fusanori Nishimura, Takayoshi Yamaza. Interferon-gamma improves impaired dentinogenic and immunosuppressive functions of irreversible pulpitis-derived human dental pulp stem cells. Scientific Reports. Nature publishing group. 6, Article number: 19286. 2016.

Papers

  • NaV1.1 contributes to the cell cycle of human mesenchymal stem cells by regulating AKT and CDK2 Reviewed

    Mohammed Fouad Zakaria, Hiroki Kato, Soichiro Sonoda, Kenichi Kato, Norihisa Uehara, Yukari Kyumoto-Nakamura, Mohammed Majd Sharifa, Liting Yu, Lisha Dai, Haruyoshi Yamaza, Shunichi Kajioka, Fusanori Nishimura, Takayoshi Yamaza

    Journal of Cell Science   2024.9   （ ISSN:0021-9533 eISSN:1477-9137 ）

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    Language：English   Publishing type：Research paper (scientific journal)   Publisher：The Company of Biologists  

    Non-excitable cells express sodium voltage-gated channel alpha subunit 1 gene and protein (SCN1A/NaV1.1); however, the functions of NaV1.1 are unclear. SCN1A was expressed in human mesenchymal stem cells (MSCs). Nav1.1 was abundantly expressed in the endoplasmic reticulum of MSCs; however, its expression was not found to be related to sodium currents. SCN1A-silencing reduced MSC proliferation and delayed the cell cycle in the S phase. SCN1A-silencing also suppressed the protein levels of CDK2 and AKT, despite similar mRNA expression, and inhibited AKT phosphorylation in MSCs. Cycloheximide-chase assay showed that SCN1A-silencing induced CDK2 but not AKT protein degradation in MSCs. Proteolysis inhibition assay using epoxomicin, bafilomycin A1, and NH4Cl, revealed that the ubiquitin-proteasome and autophagy/endo-lysosome systems were irrelevant to CDK2 and AKT protein reduction in SCN1A-silenced MSCs. AKT inhibitor LY294002 did not affect the degradation and nuclear localization of CDK2 in MSCs. Likewise, AKT activator SC79 did not attenuate the SCN1A-silencing effects on CDK2 in MSCs. These results suggest that NaV1.1 contributes to the cell cycle of MSCs by regulating the post-translational control of AKT and CDK2.

    DOI： 10.1242/jcs.261732

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  • Erythropoietin receptor signal is crucial for periodontal ligament stem cell-based tissue reconstruction in periodontal disease Reviewed

    Zakaria MHD. Fouad, Sonoda Soichiro, Kato Hiroki, Ma Lan, Uehara Norihisa, Kyumoto Yukari, Sharifa M. Majd, Yu Liting, Dai Lisha, Yamauchi Erika, Aijima Reona, Yamaza Haruyoshi, Nishimura Fusanori, Yamaza Takayoshi

    Scientific Reports   14   6719   2024.3   （ eISSN:20452322 ）

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    Alveolar bone loss caused by periodontal disease eventually leads to tooth loss. Periodontal ligament stem cells (PDLSCs) are the tissue-specific cells for maintaining and repairing the periodontal ligament, cementum, and alveolar bone. Here, we investigated the role of erythropoietin receptor (EPOR), which regulates the microenvironment-modulating function of mesenchymal stem cells, in PDLSC-based periodontal therapy. We isolated PDLSCs from patients with chronic periodontal disease and healthy donors, referred to as PD-PDLSCs and Cont-PDLSCs, respectively. PD-PDLSCs exhibited reduced potency of periodontal tissue regeneration and lower expression of EPOR compared to Cont-PDLSCs. EPOR-silencing suppressed the potency of Cont-PDLSCs mimicking PD-PDLSCs, whereas EPO-mediated EPOR activation rejuvenated the reduced potency of PD-PDLSCs. Furthermore, we locally transplanted EPOR-silenced and EPOR-activated PDLSCs into the gingiva around the teeth of ligament-induced periodontitis model mice and demonstrated that EPOR in PDLSCs participated in the regeneration of the periodontal ligament, cementum, and alveolar bone in the ligated teeth. The EPOR-mediated paracrine function of PDLSCs maintains periodontal immune suppression and bone metabolic balance via osteoclasts and osteoblasts in the periodontitis model mice. Taken together, these results suggest that EPOR signaling is crucial for PDLSC-based periodontal regeneration and paves the way for the development of novel options for periodontal therapy.

    CiNii Research

  • Bone metastatic mammary tumor cell-derived extracellular vesicles inhibit osteoblast maturation via JNK signaling. Reviewed

    Norihisa Uehara, Shibusawa N, Mikami Y, Kyumoto-Nakamura Y, Sonoda S, Kato H, Yamaza T, Kukita T

    Archives of biochemistry and biophysics   750   109821   2023.11   （ ISSN:0003-9861 eISSN:1096-0384 ）

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    The metastases of breast cancer to bone often cause osteolytic lesions not only by stimulating osteoclasts to resorb the bone but also by inhibiting osteoblasts from bone formation. Although tumor cell-derived extracellular vesicles (EVs) promote osteoclast differentiation and bone resorption, their roles in osteoblast differentiation and functions have not been elucidated. In this study, we investigated the effects of breast cancer cell-derived EVs on osteoblast differentiation and functions in vitro. We found that upon osteogenic induction, 4T1 bone metastatic mouse mammary tumor cell-derived EVs (4T1-EVs) were inhibited matrix mineralization of ST2 mouse bone marrow stromal cells. Temporal expression analysis of osteoblast marker genes, including runt-related transcription factor 2 (Runx2), osterix (Osx), alkaline phosphatase (Alp), collagen type I (Col1a1), bone sialoprotein (Bsp), and osteocalcin (Bglap) revealed that 4T1-EVs decreased their expression during the late stage of osteoblast differentiation. Elevated levels of c-Jun N-terminal kinase (JNK) phosphorylation, upon osteogenic induction, were diminished by 4T1-EVs, significantly. In contrast, the nullification of reduced JNK phosphorylation by anisomycin, a potent JNK activator, increased the expression levels of osteoblast differentiation markers. Overall, our data indicated that 4T1-EVs affect osteoblast maturation, at least partially, through the regulation of JNK activity, which provides novel insights into the pathological impact of osteolytic bone metastasis and the role of EVs in osteoblast differentiation.

    DOI： 10.1016/j.abb.2023.109821

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  • Cutting-edge regenerative therapy for Hirschsprung disease and its allied disorders. Reviewed

    Koichiro Yoshimaru, Toshiharu Matsuura, Yasuyuki Uchida, Soichiro Sonoda, Shohei Maeda, Keisuke Kajihara, Yuki Kawano, Takeshi Shirai, Yukihiro Toriigahara, Alvin Santoso Kalim, Xiu-Ying Zhang, Yoshiaki Takahashi, Naonori Kawakubo, Kouji Nagata, Haruyoshi Yamaza, Takayoshi Yamaza, Tomoaki Taguchi, Tatsuro Tajiri

    Surgery today   54 ( 9 )   977 - 994   2023.9   （ ISSN:0941-1291 eISSN:1436-2813 ）

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

    Hirschsprung disease (HSCR) and its associated disorders (AD-HSCR) often result in severe hypoperistalsis caused by enteric neuropathy, mesenchymopathy, and myopathy. Notably, HSCR involving the small intestine, isolated hypoganglionosis, chronic idiopathic intestinal pseudo-obstruction, and megacystis-microcolon-intestinal hypoperistalsis syndrome carry a poor prognosis. Ultimately, small-bowel transplantation (SBTx) is necessary for refractory cases, but it is highly invasive and outcomes are less than optimal, despite advances in surgical techniques and management. Thus, regenerative therapy has come to light as a potential form of treatment involving regeneration of the enteric nervous system, mesenchyme, and smooth muscle in affected areas. We review the cutting-edge regenerative therapeutic approaches for managing HSCR and AD-HSCR, including the use of enteric nervous system progenitor cells, embryonic stem cells, induced pluripotent stem cells, and mesenchymal stem cells as cell sources, the recipient intestine's microenvironment, and transplantation methods. Perspectives on the future of these treatments are also discussed.

    DOI： 10.1007/s00595-023-02741-6

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  • Extracellular vesicles rejuvenate the microenvironmental modulating function of recipient tissue-specific mesenchymal stem cells in osteopenia treatment. Reviewed International journal

    Soichiro Sonoda, Takayoshi Yamaza

    Frontiers in endocrinology   14   1151429 - 1151429   2023.3   （ ISSN:1664-2392 ）

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

    Systemic transplantation of mesenchymal stem cells (MSCs), such as bone marrow MSCs (BMMSCs) and stem cells from human exfoliated deciduous teeth (SHED), is considered a prominent treatment for osteopenia. However, the mechanism of action of the transplanted MSCs has been poorly elucidated. In the recipient target tissue, including bone and bone marrow, only a few donor MSCs can be detected, suggesting that the direct contribution of donor MSCs may not be expected for osteopenia treatment. Meanwhile, secretomes, especially contents within extracellular vesicles (EVs) released from donor MSCs (MSC-EVs), play key roles in the treatment of several diseases. In this context, administrated donor MSC-EVs may affect bone-forming function of recipient cells. In this review, we discuss how MSC-EVs contribute to bone recovery recipient tissue in osteopenia. We also summarize a novel mechanism of action of systemic administration of SHED-derived EVs (SHED-EVs) in osteopenia. We found that reduced telomerase activity in recipient BMMSCs caused the deficiency of microenvironmental modulating function, including bone and bone marrow-like niche formation and immunomodulation in estrogen-deficient osteopenia model mice. Systemic administration of SHED-EVs could exert therapeutic effects on bone reduction via recovering the telomerase activity, leading to the rejuvenation of the microenvironmental modulating function in recipient BMMSCs, as seen in systemic transplantation of SHED. RNase-preconditioned donor SHED-EVs diminished the therapeutic benefits of administrated SHED-EVs in the recipient osteopenia model mice. These facts suggest that MSC-EV therapy targets the recipient BMMSCs to rejuvenate the microenvironmental modulating function via telomerase activity, recovering bone density. We then introduce future challenges to develop the reproducible MSC-EV therapy in osteopenia.

    DOI： 10.3389/fendo.2023.1151429

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  • Targeting hepatic oxidative stress rescues bone loss in liver fibrosis Reviewed

    Soichiro Sonoda, Sara Murata, Haruyoshi Yamaza, Ratih Yuniartha, Junko Fujiyoshi, Koichiro Yoshimaru, Toshiharu Matsuura, Yoshinao Oda, Shouichi Ohga, Tasturo Tajiri, Tomoaki Taguchi, Takayoshi Yamaza

    Molecular Metabolism   66   101599   2022.12   （ ISSN:2212-8778 eISSN:2212-8778 ）

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    Objective: Chronic liver diseases often involve metabolic damage to the skeletal system. The underlying mechanism of bone loss in chronic liver diseases remains unclear, and appropriate therapeutic options, except for orthotopic liver transplantation, have proved insufficient for these patients. This study aimed to investigate the efficacy and mechanism of transplantation of immature hepatocyte-like cells converted from stem cells from human exfoliated deciduous teeth (SHED-Heps) in bone loss of chronic liver fibrosis. Methods: Mice that were chronically treated with CCl4 received SHED-Heps, and trabecular bone density, reactive oxygen species (ROS), and osteoclast activity were subsequently analyzed in vivo and in vitro. The effects of stanniocalcin 1 (STC1) knockdown in SHED-Heps were also evaluated in chronically CCl4 treated mice. Results: SHED-Hep transplantation (SHED-HepTx) improved trabecular bone loss and liver fibrosis in chronic CCl4-treated mice. SHED-HepTx reduced hepatic ROS production and interleukin 17 (Il-17) expression under chronic CCl4 damage. SHED-HepTx reduced the expression of both Il-17 and tumor necrosis factor receptor superfamily 11A (Tnfrsf11a) and ameliorated the imbalance of osteoclast and osteoblast activities in the bone marrow of CCl4-treated mice. Functional knockdown of STC1 in SHED-Heps attenuated the benefit of SHED-HepTx including anti-bone loss effect by suppressing osteoclast differentiation through TNFSF11–TNFRSF11A signaling and enhancing osteoblast differentiation in the bone marrow, as well as anti-fibrotic and anti-ROS effects in the CCl4-injured livers. Conclusions: These findings suggest that targeting hepatic ROS provides a novel approach to treat bone loss resulting from chronic liver diseases.

    DOI： 10.1016/j.molmet.2022.101599

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  • miR-92a-3p encapsulated in bone metastatic mammary tumor cell–derived extracellular vesicles modulates mature osteoclast longevity Reviewed

    Norihisa Uehara, Yukari Kyumoto-Nakamura, Yoshikazu Mikami, Manabu Hayatsu, Soichiro Sonoda, Takayoshi Yamaza, Akiko Kukita, Toshio Kukita

    Cancer Science   113 ( 12 )   4219 - 4229   2022.12   （ ISSN:1347-9032 eISSN:1349-7006 ）

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    Aberrant osteoclast formation and activation are the hallmarks of osteolytic metastasis. Extracellular vesicles (EVs), released from bone metastatic tumor cells, play a pivotal role in the progression of osteolytic lesions. However, the mechanisms through which tumor cell–derived EVs regulate osteoclast differentiation and function have not been fully elucidated. In this study, we found that 4T1 bone metastatic mouse mammary tumor cell–derived EVs (4T1-EVs) are taken up by mouse bone marrow macrophages to facilitate osteoclastogenesis. Furthermore, treatment of mature osteoclasts with 4T1-EVs promoted bone resorption, which was accompanied by enhanced survival of mature osteoclasts through the negative regulation of caspase-3. By comparing the miRNA content in 4T1-EVs with that in 67NR nonmetastatic mouse mammary tumor cell–derived EVs (67NR-EVs), miR-92a-3p was identified as one of the most enriched miRNAs in 4T1-EVs, and its transfer into mature osteoclasts significantly reduced apoptosis. Bioinformatic and Western blot analyses revealed that miR-92a-3p directly targeted phosphatase and tensin homolog (PTEN) in mature osteoclasts, resulting in increased levels of phospho-Akt. Our findings provide novel insights into the EV-mediated regulation of osteoclast survival through the transfer of miR-92a-3p, which enhances mature osteoclast survival via the Akt survival signaling pathway, thus promoting bone resorption.

    DOI： 10.1111/cas.15557

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  • 骨転移乳癌細胞由来細胞外小胞に封入されたmiR-92a-3pは成熟破骨細胞の寿命を調節する(miR-92a-3p encapsulated in bone metastatic mammary tumor cell-derived extracellular vesicles modulates mature osteoclast longevity) Reviewed

    Uehara Norihisa, Kyumoto-Nakamura Yukari, Mikami Yoshikazu, Hayatsu Manabu, Sonoda Soichiro, Yamaza Takayoshi, Kukita Akiko, Kukita Toshio

    Cancer Science   113 ( 12 )   4219 - 4229   2022.12   （ ISSN:1347-9032 ）

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    Language：English   Publisher：John Wiley & Sons Australia, Ltd  

    骨転移乳癌細胞由来細胞外小胞(EV)が破骨細胞の分化や機能に及ぼす影響とそのメカニズムについて検討した。マウス乳癌細胞株4T1由来EV(4T1-EV)がマウス骨髄マクロファージに取り込まれ、破骨細胞形成を促進することを見出した。成熟破骨細胞を4T1-EVで処理すると、骨吸収が促進され、カスパーゼ3を負に制御して成熟破骨細胞の生存が促進された。4T1-EVと非転移性マウス乳癌細胞株67NR由来EV(67NR-EV)におけるmiRNAの内容を比較した。その結果、miR-92a-3pが4T1-EVに最も濃縮されたmiRNAの一つとして特定され、miR-92a-3pの成熟破骨細胞への移入によりアポトーシスが著しく抑制された。さらに、miR-92a-3pは成熟破骨細胞においてphosphatase and tensin homolog(PTEN)を直接標的とし、リン酸化Aktのレベルを増加させた。以上より、マウス乳癌細胞株4T1由来EVに存在するmiR-92a-3pは、Akt生存シグナル経路を介して成熟破骨細胞の生存を高め、骨吸収を促進させることが示された。

  • Protocol to generate xenogeneic-free/serum-free human dental pulp stem cells Reviewed

    Soichiro Sonoda, Haruyoshi Yamaza, Koichiro Yoshimaru, Tomoaki Taguchi, Takayoshi Yamaza

    STAR Protocols   3 ( 2 )   101386   2022.6   （ ISSN:2666-1667 eISSN:2666-1667 ）

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    Human dental pulp stem cell (hDPSCs)-based therapy is a feasible option for regenerative medicine, such as dental pulp regeneration. Here, we show the steps needed to colony-forming unit-fibroblasts (CFU-F)-based isolation, expansion, and cryopreservation of hDPSCs for manufacturing clinical-grade products under a xenogeneic-free/serum-free condition. We also demonstrate the characterization of hDPSCs by CFU-F, flow cytometric, and in vitro multipotent assays. For complete details on the use and execution of this protocol, please refer to Iwanaka et al. (2020).

    DOI： 10.1016/j.xpro.2022.101386

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  • Dental pulp stem cells as a therapy for congenital entero-neuropathy Reviewed

    Koichiro Yoshimaru, Takayoshi Yamaza, Shunichi Kajioka, Soichiro Sonoda, Yusuke Yanagi, Toshiharu Matsuura, Junko Yoshizumi, Yoshinao Oda, Naoko Iwata, Chiho Takai, Shinsuke Nakayama, Tomoaki Taguchi

    Scientific Reports   12 ( 1 )   6990   2022.4   （ ISSN:2045-2322 eISSN:2045-2322 ）

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    Hirschsprung’s disease is a congenital entero-neuropathy that causes chronic constipation and intestinal obstruction. New treatments for entero-neuropathy are needed because current surgical strategies have limitations5. Entero-neuropathy results from enteric nervous system dysfunction due to incomplete colonization of the distal intestine by neural crest-derived cells. Impaired cooperation between the enteric nervous system and intestinal pacemaker cells may also contribute to entero-neuropathy. Stem cell therapy to repair these multiple defects represents a novel treatment approach. Dental pulp stem cells derived from deciduous teeth (dDPSCs) are multipotent cranial neural crest-derived cells, but it remains unknown whether dDPSCs have potential as a new therapy for entero-neuropathy. Here we show that intravenous transplantation of dDPSCs into the Japanese Fancy-1 mouse, an established model of hypoganglionosis and entero-neuropathy, improves large intestinal structure and function and prolongs survival. Intravenously injected dDPSCs migrate to affected regions of the intestine through interactions between stromal cell-derived factor-1α and C-X-C chemokine receptor type-4. Transplanted dDPSCs differentiate into both pacemaker cells and enteric neurons in the proximal colon to improve electrical and peristaltic activity, in addition to their paracrine effects. Our findings indicate that transplanted dDPSCs can differentiate into different cell types to correct entero-neuropathy-associated defects.

    DOI： 10.1038/s41598-022-10077-3

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  • A New Target of Dental Pulp-Derived Stem Cell-Based Therapy on Recipient Bone Marrow Niche in Systemic Lupus Erythematosus Reviewed

    Soichiro Sonoda, Takayoshi Yamaza

    International Journal of Molecular Sciences   23 ( 7 )   2022.4   （ ISSN:1661-6596 eISSN:1422-0067 ）

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    Recent advances in mesenchymal stem/stromal cell (MSC) research have led us to con-sider the feasibility of MSC-based therapy for various diseases. Human dental pulp-derived MSCs (hDPSCs) have been identified in the dental pulp tissue of deciduous and permanent teeth, and they exhibit properties with self-renewal and in vitro multipotency. Interestingly, hDPSCs exhibit superior immunosuppressive functions toward immune cells, especially T lymphocytes, both in vitro and in vivo. Recently, hDPSCs have been shown to have potent immunomodulatory functions in treating systemic lupus erythematosus (SLE) in the SLE MRL/lpr mouse model. However, the mechanisms underlying the immunosuppressive efficacy of hDPSCs remain unknown. This review aims to introduce a new target of hDPSC-based therapy on the recipient niche function in SLE.

    DOI： 10.3390/ijms23073479

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  • Biliary atresia-specific deciduous pulp stem cells feature biliary deficiency. Reviewed International journal

    Soichiro Sonoda, Koichiro Yoshimaru, Haruyoshi Yamaza, Ratih Yuniartha, Toshiharu Matsuura, Erika Yamauchi-Tomoda, Sara Murata, Kento Nishida, Yoshinao Oda, Shouichi Ohga, Tasturo Tajiri, Tomoaki Taguchi, Takayoshi Yamaza

    Stem cell research & therapy   12 ( 1 )   582 - 582   2021.11

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    DOI： 10.1186/s13287-021-02652-8

  • Modulation of osteoclastogenesis through adrenomedullin receptors on osteoclast precursors: initiation of differentiation by asymmetric cell division Reviewed

    Toshio Kukita, Hidenobu Hiura, Jiong-Yan Gu, Jing-Qi Zhang, Yukari Kyumoto-Nakamura, Norihisa Uehara, Sara Murata, Soichiro Sonoda, Takayoshi Yamaza, Ichiro Takahashi, Akiko Kukita

    Laboratory Investigation   101 ( 11 )   1449 - 1457   2021.10

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    DOI： 10.1038/s41374-021-00633-2

  • Targeting of deciduous tooth pulp stem cell-derived extracellular vesicles on telomerase-mediated stem cell niche and immune regulation in systemic lupus erythematosus Reviewed

    Soichiro Sonoda, Sara Murata, Hiroki Kato, Fouad Zakaria, Yukari Kyumoto-Nakamura, Norihisa Uehara, Haruyoshi Yamaza, Toshio Kukita, Takayoshi Yamaza

    Journal of Immunology   206 ( 12 )   3053 - 3063   2021.6

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    DOI： 10.4049/jimmunol.2001312

  • Cholangiogenic potential of human deciduous pulp stem cell-converted hepatocyte-like cells Reviewed International journal

    Ratih Yuniartha, Takayoshi Yamaza, Soichiro Sonoda, Koichiro Yoshimaru, Toshiharu Matsuura, Haruyoshi Yamaza, Yoshinao Oda, Shouichi Ohga, Tomoaki Taguchi

    Stem Cell Research & Therapy   12 ( 1 )   57 - 57   2021.1

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    DOI： 10.1186/s13287-020-02113-8

  • Extracellular vesicles from deciduous pulp stem cells recover bone loss by regulating telomerase activity in an osteoporosis mouse model Reviewed

    Soichiro Sonoda, Sara Murata, Kento Nishida, Hiroki Kato, Norihisa Uehara, Yukari N. Kyumoto, Haruyoshi Yamaza, Ichiro Takahashi, Toshio Kukita, Takayoshi Yamaza

    Stem Cell Research and Therapy   11 ( 1 )   2020.7

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    DOI： 10.1186/s13287-020-01818-0

  • A model study for the manufacture and validation of clinical-grade deciduous dental pulp stem cells for chronic liver fibrosis treatment Reviewed

    Tsuyoshi Iwanaka, Takayoshi Yamaza, Soichiro Sonoda, Koichiro Yoshimaru, Toshiharu Matsuura, Haruyoshi Yamaza, Shouichi Ohga, Yoshinao Oda, Tomoaki Taguchi

    Stem Cell Research and Therapy   11 ( 1 )   2020.3

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    DOI： 10.1186/s13287-020-01630-w

  • Therapeutic potential of hepatocyte-like-cells converted from stem cells from human exfoliated deciduous teeth in fulminant Wilson’s disease Reviewed

    9 ( 1 )   2019.12

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    Wilson’s disease (WD) is an inherited metabolic disease arising from ATPase copper transporting beta gene (ATP7B) mutation. Orthotoropic liver transplantation is the only radical treatment of fulminant WD, although appropriate donors are lacking at the onset of emergency. Given the hepatogenic capacity and tissue-integration/reconstruction ability in the liver of stem cells from human exfoliated deciduous teeth (SHED), SHED have been proposed as a source for curing liver diseases. We hypothesized the therapeutic potential of SHED and SHED-converted hepatocyte-like- cells (SHED-Heps) for fulminant WD. SHED and SHED-Heps were transplanted into WD model Atp7b-mutated Long-Evans Cinnamon (LEC) rats received copper overloading to induce a lethal fulminant liver failure. Due to the superior copper tolerance via ATP7B, SHED-Hep transplantation gave more prolonged life-span of fulminant LEC rats than SHED transplantation. The integrated ATP7B-expressing SHED-Heps showed more therapeutic effects on to restoring the hepatic dysfunction and tissue damages in the recipient liver than the integrated naïve SHED without ATP7B expression. Moreover, SHED-Heps could reduce copper-induced oxidative stress via ATP7B- independent stanniocalcin 1 secretion in the fulminant LEC rats, suggesting a possible role for paracrine effect of the integrated SHED-Heps. Taken together, SHED-Heps offer a potential of functional restoring, bridging, and preventive approaches for treating fulminant WD.

    DOI： 10.1038/s41598-018-38275-y

  • Therapeutic potential of spheroids of stem cells from human exfoliated deciduous teeth for chronic liver fibrosis and hemophilia A Reviewed

    Yoshiaki Takahashi, Ratih Yuniartha, Takayoshi Yamaza, Soichiro Sonoda, Haruyoshi Yamaza, Kosuke Kirino, Koichiro Yoshimaru, Toshiharu Matsuura, Tomoaki Taguchi

    Pediatric Surgery International   35 ( 12 )   1379 - 1388   2019.12

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    DOI： 10.1007/s00383-019-04564-4

  • Osteoblast lineage-specific cell-surface antigen (A7) regulates osteoclast recruitment and calcification during bone remodeling Reviewed

    Tamer Badawy, Yukari Kyumoto-Nakamura, Norihisa Uehara, Jingqi Zhang, Soichiro Sonoda, Hidenobu Hiura, Takayoshi Yamaza, Akiko Kukita, Toshio Kukita

    Laboratory Investigation   99 ( 6 )   866 - 884   2019.6

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    DOI： 10.1038/s41374-018-0179-4

  • Acetylsalicylic Acid Treatment and Suppressive Regulation of AKT Accelerate Odontogenic Differentiation of Stem Cells from the Apical Papilla Reviewed

    Yosuke Tanaka, Soichiro Sonoda, Haruyoshi Yamaza, Sara Murata, Kento Nishida, Yukari Kyumoto-Nakamura, Norihisa Uehara, Kazuaki Nonaka, Toshio Kukita, Takayoshi Yamaza

    Journal of Endodontics   45 ( 5 )   591 - 598.e6   2019.5

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    DOI： 10.1016/j.joen.2019.01.016

  • Exogenous nitric oxide stimulates the odontogenic differentiation of rat dental pulp stem cells Reviewed

    Soichiro Sonoda, Yu Feng Mei, Ikiru Atsuta, Atsushi Danjo, Haruyoshi Yamaza, Shion Hama, Kento Nishida, Ronghao Tang, Yukari Kyumoto-Nakamura, Norihisa Uehara, Toshio Kukita, Fusanori Nishimura, Takayoshi Yamaza

    Scientific Reports   8 ( 1 )   2018.12

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    DOI： 10.1038/s41598-018-21183-6

  • Pamidronate decreases bilirubin-impaired cell death and improves dentinogenic dysfunction of stem cells from human deciduous teeth Reviewed

    Haruyoshi Yamaza, Soichiro Sonoda, Kazuaki Nonaka, Toshio Kukita, Takayoshi Yamaza

    Stem Cell Research and Therapy   9 ( 1 )   2018.11

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    DOI： 10.1186/s13287-018-1042-7

  • Suppression of AKT-mTOR signal pathway enhances osteogenic/dentinogenic capacity of stem cells from apical papilla Reviewed

    Yosuke Tanaka, Soichiro Sonoda, Haruyoshi Yamaza, Sara Murata, Kento Nishida, Shion Hama, Yukari Kyumoto-Nakamura, Norihisa Uehara, Kazuaki Nonaka, Toshio Kukita, Takayoshi Yamaza

    Stem Cell Research and Therapy   9 ( 1 )   2018.11

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

    DOI： 10.1186/s13287-018-1077-9

  • Bilirubin reversibly affects cell death and odontogenic capacity in stem cells from human exfoliated deciduous teeth Reviewed

    H. Yamaza, E. Tomoda, S. Sonoda, K. Nonaka, T. Kukita, T. Yamaza

    Oral Diseases   24 ( 5 )   809 - 819   2018.7

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

    DOI： 10.1111/odi.12827

  • Unique Osteoblast-Specific Cell-Surface Antigen Useful for Odontoblast Ontology and Dentin Regeneration Reviewed

    Tamer Badawy, Yukari Kyumoto Nakamura, Norihisa Uehara, Jingqi Zhang, Hidenobu Hiura, Soichiro Sonoda, Takayoshi Yamaza, Akiko Kukita, Toshio Kukita

    Oral Health & Dental Science   2 ( 2 )   1 - 7   2018.6

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

    DOI： 10.33425/2639-9490.1018

  • Interferon-gamma improves impaired dentinogenic and immunosuppressive functions of irreversible pulpitis-derived human dental pulp stem cells Reviewed

    Soichiro Sonoda, Haruyoshi Yamaza, Lan Ma, Yosuke Tanaka, Erika Tomoda, Reona Aijima, Kazuaki Nonaka, Toshio Kukita, Songtao Shi, Fusanori Nishimura, Takayoshi Yamaza

    Scientific Reports   6   2016.1

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

    DOI： 10.1038/srep19286

  • Transplantation of mesenchymal stem cells ameliorates secondary osteoporosis through interleukin-17-impaired functions of recipient bone marrow mesenchymal stem cells in MRL/lpr mice Reviewed

    Lan Ma, Reona Aijima, Yoshihiro Hoshino, Haruyoshi Yamaza, Erika Tomoda, Yosuke Tanaka, Soichiro Sonoda, Guangtai Song, Wei Zhao, Kazuaki Nonaka, Songtao Shi, Takayoshi Yamaza

    Stem Cell Research and Therapy   6 ( 1 )   2015.5

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

    DOI： 10.1186/s13287-015-0091-4

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Presentations

  • 胸腺間葉系ストロマ細胞による内在性制御性T細胞の産生メカニズムの解明

    園田 聡一朗、久本 由香里、加藤 大樹、上 原 範久、山座 孝義

    第65回歯科基礎医学会学術大会  2023.9 

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    Event date： 2023.9

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：日本大学歯学部（東京都千代田区）   Country：Japan  

  • 乳歯幹細胞の細胞外小胞による宿主間葉系幹細胞を標的とした全身性エリテマトーデス治療メカニズムの解明

    園田 聡一朗, 山座 孝義

    第21回日本再生医療学会総会  2022.3 

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    Event date： 2022.3

    Language：Japanese  

    Country：Other  

  • 乳歯幹細胞の細胞外小胞による宿主間葉系幹細胞を標的とした全身性エリテマトーデス治療メカニズムの解明

    園田 聡一朗, 山座 孝義

    第21回日本再生医療学会総会  2022.3 

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    Event date： 2022.3

    Language：Japanese   Presentation type：Oral presentation (general)  

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  • Extracellular vesicles-mediated novel therapeutic mechanism of deciduous toot pulp stem cell-based therapy for systemic lupus erythematosus

    2021.10 

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    Event date： 2021.10

    Language：English  

    Country：Other  

    Extracellular vesicles-mediated novel therapeutic mechanism of deciduous toot pulp stem cell-based therapy for systemic lupus erythematosus

  • 乳歯幹細胞の細胞外小胞を介した全身性エリテマトーデスの新規治療メカニズムの解明

    園田 聡一朗, 山座 孝義

    第63回歯科基礎医学会学術大会  2021.10 

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    Event date： 2021.10

    Language：English  

    Country：Other  

  • 胆道閉鎖症患児由来乳歯幹細胞の細胞移植治療効果低下をもたらす機構の解析

    園田 聡一朗, 村田 早羅, 加藤 大樹, 久本 由香里, 上原 範久, 久木田 敏夫, 山座 孝義

    第62回歯科基礎医学会学術大会  2020.9 

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    Event date： 2020.10

    Language：Others  

    Country：Other  

  • 胆道閉鎖症患児由来乳歯幹細胞の細胞移植治療効果低下をもたらす機構の解析

    園田 聡一朗, 村田 早羅, 加藤 大樹, 久本 由香里, 上原 範久, 久木田 敏夫, 山座 孝義

    第62回歯科基礎医学会学術大会  2020.9 

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    Event date： 2020.10

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  • 胆道閉鎖症由来乳歯幹細胞の特性とその肝再生能力

    園田 聡一朗, 村田 早羅, 山座 孝義

    日本再生医療学会  2020.5 

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    Event date： 2020.5

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：オンライン   Country：Japan  

  • 胆道閉鎖症患児に対する自家乳歯幹細胞移植治療を目指した基礎研究

    園田 聡一朗, 村田 早羅, 久本 由香里, 上原 範久, 久木田 敏夫, 山座 孝義

    歯科基礎医学会  2019.10 

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    Event date： 2019.10

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：東京医科歯科大学   Country：Japan  

  • Improvement of dentinogenesis of Irreversible pulpitis-derived DPSCs. International conference

    Soichiro Sonoda, Takayoshi Yamaza, Yusuke Makino, La Ma, Toshio Kukita.

    The 59th Annual Meeting of Japanese Association for Dental Research.  2011.6 

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    Event date： 2019.6

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

    Country：Japan  

  • 非可逆性炎歯髄由来幹細胞は歯髄再生治療に応用可能か？

    園田聡一朗, 山座孝義, 久木田敏夫.

    第57回歯科基礎医学会学術大会・総会.  2015.9 

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    Event date： 2019.6

    Language：Japanese  

    Country：Japan  

  • Interferon-gamma improves impaired dentinogenic function and immunosuppressive properties in irreversible pulpitis-derived human dental pulp stem cells. International conference

    Soichiro Sonoda, Erika Tomoda, Yosuke Tanaka, Fusanori Nishimura, Takayoshi Yamaza.

    he 63rd Annual Meeting of Japanese Association for Dental Research.  2015.10 

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    Event date： 2019.6

    Language：English  

    Country：Japan  

  • 炎症性サイトカイン刺激による不可逆性歯髄炎組織由来歯髄幹細胞の象牙質形成能ならびに免疫抑制能の改善.

    園田聡一朗, 山座孝義, 西村英紀.

    日本歯周病学会九州五大学・日本臨床歯周病学会九州支部 合同研修会.  2015.11 

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    Event date： 2019.6

    Language：Japanese  

    Country：Japan  

  • Patient-derived dental pulp stem cells based regeneration of dentin/pulp-complex. International conference

    Soichiro Sonoda, Takayoshi Yamaza, Fusanori Nishimura.

    Kyudai Oral Bioscience  2016.2 

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    Event date： 2019.6

    Language：English  

    Country：Japan  

  • 不可逆性歯髄炎組織由来歯髄幹細胞を応用した象牙質／歯髄複合体の再生.

    園田聡一朗, 山座孝義, 西村英紀.

    第144回日本歯科保存学会春季学術大会.  2016.6 

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    Event date： 2019.6

    Language：Japanese  

    Country：Japan  

  • 一酸化窒素によるラット歯髄幹細胞の象牙芽細胞分化促進.

    園田聡一朗, 山座孝義, 友田恵利佳, 田中陽介, 久木田敏夫.

    第58回歯科基礎医学会学術大会・総会.  2016.8 

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    Event date： 2019.6

    Language：Japanese  

    Venue：札幌コンベンションセンター. 北海道.   Country：Japan  

  • 一酸化窒素によるラット歯髄幹細胞の象牙質形成促進.

    園田聡一朗, 山座孝義, 久木田敏夫.

    第73回日本解剖学会九州支部学術集会.  2017.10 

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    Event date： 2019.6

    Language：Japanese  

    Venue：都久志会館. 福岡.   Country：Japan  

  • 外因性の一酸化窒素刺激は歯髄幹細胞の象牙芽細胞分化を促進する

    園田聡一朗, 山座孝義, 西村英紀

    歯科保存学会2018春季大会  2018.6 

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    Event date： 2019.6

    Language：Japanese  

    Country：Japan  

  • 乳歯幹細胞の単離時に血清濃度が与える影響について

    園田 聡一朗, 大谷 憲司, 山座 孝義

    第60回日本歯科基礎医学会総会  2018.9 

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    Event date： 2019.6

    Language：Japanese  

    Country：Japan  

  • 骨転移性乳癌細胞由来細胞外小胞に内包されるmiR-92a-3pは成熟破骨細胞の生存を促進する(Bone metastatic mammary tumor cell-derived extracellular vesicles promote mature osteoclast longevity)

    上原 範久, 久本 由香里, 三上 剛和, 園田 聡一朗, 山座 孝義, 久木田 敏夫

    日本癌学会総会記事  2023.9  (一社)日本癌学会

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    Language：English  

  • 胸腺間葉系ストロマ細胞による内在性制御性T細胞の産生メカニズムの解明

    園田 聡一朗, 久本 由香里, 加藤 大樹, 上原 範久, 山座 孝義

    Journal of Oral Biosciences Supplement  2023.9  (一社)歯科基礎医学会

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    Language：Japanese  

  • 根尖歯乳頭組織由来幹細胞に発現する転写因子PITX2の機能解析

    久本 由香里, 園田 聡一朗, 加藤 大樹, 上原 範久, 山座 孝義

    Journal of Oral Biosciences Supplement  2023.9  (一社)歯科基礎医学会

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    Language：Japanese  

  • 小児外科における最先端医療の現状と展望【International】ヒト脱落乳歯歯髄幹細胞移植によるhypoganglionosisに対する新規治療法開発

    吉丸 耕一朗, 園田 聡一朗, 山内 恵利佳, 河野 淳, 松浦 俊治, 山座 孝義, 小田 義直, 田尻 達郎, 田口 智章

    日本外科学会定期学術集会抄録集  2022.4  (一社)日本外科学会

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    Language：Japanese  

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MISC

  • 疾患特異的乳歯幹細胞モデルによる胆管症の病因解明

    園田 聡一朗, 吉丸 耕一朗, 田口 智章, 山座 孝義

    細胞   56 ( 10 )   747 - 749   2024.9   （ ISSN:1346-7557 ）

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    Language：Japanese   Publisher：(株)ニュー・サイエンス社  

    胆道閉鎖症Biliary Atresia(BA)は,肝外胆管の閉塞によって胆汁がうっ滞する難病であるが,その病因は不明である。乳歯歯髄の体性幹細胞である乳歯幹細胞Stem Cells from Exfoliated Deciduous Teeth(SHED)は,その発生学的起源ゆえ,胎児組織幹細胞でもある。そのため,胎児期の母体内で生じる大きなエピジェネティック変化を記憶している可能性が推測される。四塩化炭素誘導性肝障害モデルマウスを用いたSHED注入実験において,SHEDは,レシピエント肝組織で肝細胞様細胞と胆管様構造を呈する胆管上皮細胞様細胞に分化した。しかし,BA特異的SHEDは,肝細胞様細胞に分化したが,胆管上皮細胞様細胞には分化しなかった。また,ドナー由来の肝芽細胞もレシピエント肝組織で確認できた。したがって,BAの発症機序として,母体内の誘発因子が,肝芽細胞から胆管形成を抑制するのではないかと仮説した。現在,筆者らは,疾患特異的SHEDを用いた研究モデルで,BAなどの胆管症発症分子機序の解明を試みている。(著者抄録)

  • Extracellular vesicles rejuvenate the microenvironmental modulating function of recipient tissue-specific mesenchymal stem cells in osteopenia treatment. Reviewed

    Soichiro Sonoda, Takayoshi Yamaza

    Frontiers in endocrinology   2023.3

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

    DOI： 10.3389/fendo.2023.1151429

  • 【疾患と免疫の新たな関係】歯髄幹細胞を用いたSLEの治療戦略

    山座 孝義, 園田 聡一朗

    臨床免疫・アレルギー科   77 ( 5 )   575 - 583   2022.5   （ ISSN:1881-1930 ）

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    Language：Japanese   Publisher：(有)科学評論社  

  • A New Target of Dental Pulp-Derived Stem Cell-Based Therapy on Recipient Bone Marrow Niche in Systemic Lupus Erythematosus

    Soichiro Sonoda, Takayoshi Yamaza

    International Journal of Molecular Sciences   2022.3

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    Language：Others  

    DOI： 10.3390/ijms23073479

  • Properties and Possibilities of Human Dental Pulp-Derived Stem Cells.

    Soichiro Sonoda, Erika Tomoda, Yosuke Tanaka, Takayoshi Yamaza.

    2015.2

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    Language：English  

Professional Memberships

  • 日本歯周病学会

  • 日本歯科保存学会

  • 歯科基礎医学会

  • Japanese Association of Denal Research

  • International Association of Dental research

  • 日本再生医療学会

  • 歯科基礎医学会

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  • 日本歯科保存学会

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  • 日本歯周病学会

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  • 日本再生医療学会

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  • Japanese Association of Denal Research

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  • International Association of Dental research

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Committee Memberships

  • 九州大学   OSCE委員  

    2021.4 - 2022.3   

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Research Projects

  • 胸腺髄質線維芽細胞による制御性T細胞の生成制御因子の探究

    Grant number：24K12873  2024.4 - 2027.3

    科学研究費助成事業  基盤研究(C)

    園田 聡一朗, 山座 孝義

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    Grant type：Scientific research funding

    制御性T細胞（Treg）は「免疫寛容」を実装した司令塔である。胸腺で生成される内在性Treg（nTreg）には自己抗体産生の制御に関わるサブセットが報告されており、nTregが自己免疫疾患の発症に重要な働きをもつことが示唆されている。しかし、nTregの生成メカニズムについては不明な点が多く残されている。髄質線維芽細胞（mFB）が間葉系ストロマ細胞として同定され、mFBがnTregの生成に関わる微小環境を形成する細胞として注目されている。本研究では、mFBによるnTreg生成の分子メカニズムの解明を試み、mFBを標的とした自己免疫疾患の新たな治療法の開発に向けた学術的基盤の構築を目指す。

    CiNii Research

  • 口腔がんの転移をもたらすリンパ節線維芽細胞様細網細胞の変異メカニズムの解明

    2023.4 - 2027.3

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    Authorship：Coinvestigator(s) 

  • 口腔がんの転移をもたらすリンパ節線維芽細胞様細網細胞の変異メカニズムの解明

    Grant number：23K27762  2023.4 - 2027.3

    科学研究費助成事業  基盤研究(B)

    山座 孝義, 園田 聡一朗, 久本 由香里

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    Grant type：Scientific research funding

    口腔がんのリンパ節転移は不顕性に進行し、転移後に発見されるケースが多い。患者のQOL向上のために、低侵襲的な口腔がんのリンパ節転移に対する新規治療法が必要である。センチネルリンパ節は、がん遠隔転移の防波堤である。がん転移センチネルリンパ節では、線維芽細胞様細網細胞による物質輸送系の線維化が起こり、T細胞による抗腫瘍免疫機能が低下すると考えられている。本研究では、口腔がん細胞が線維芽細胞様細網細胞を介して抗腫瘍免疫機能を抑制するメカニズムおよびセンチネルリンパ節への転移機序を解明し、センチネルリンパ節転移に対する非外科的治療法の学術的基盤の確立を目指す。

    CiNii Research

  • 口腔がんの転移をもたらすリンパ節線維芽細胞様細網細胞の変異メカニズムの解明

    Grant number：23H03071  2023 - 2026

    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：Coinvestigator(s)  Grant type：Scientific research funding

  • 疾患特異的乳歯幹細胞モデルによる胆管障害症の病態解明

    Grant number：22K19565  2022 - 2024

    日本学術振興会  科学研究費助成事業  挑戦的研究（萌芽）

    山座 孝義, 園田 聡一朗

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    Authorship：Coinvestigator(s)  Grant type：Scientific research funding

    本研究の目的は「乳歯幹細胞を用いた胆道上皮細胞分化誘導法を開発し、胆管障害患児由来の疾患特異的な乳歯幹細胞を用いて新規ex vivo解析モデルを構築すること」である。胆管障害とは胆汁の排泄障害を呈する進行性の慢性肝疾患であるが、原因・発症機構が未解明である。肝移植以外の根治治療がなく、代替となる有効な治療法の開発が責務である。申請者らは乳歯幹細胞の肝細胞分化について多数の研究成果を報告してきた。本研究ではその知見を生かし、乳歯幹細胞による胆道上皮細胞分化誘導法を開発する。さらに胆管障害の患児より乳歯幹細胞を単離し、胆管上皮細胞への分化能や機能を比較検討することで胆管障害発症機序の解明を目指す。

    CiNii Research

  • 歯髄幹細胞移植による胸腺機能の改善を介した免疫調節機序の研究

    2021.5 - 2024.3

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    Authorship：Principal investigator 

  • 歯髄幹細胞移植による胸腺機能の改善を介した免疫調節機序の研究

    Grant number：21K16932  2021 - 2023

    日本学術振興会  科学研究費助成事業  若手研究

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    Authorship：Principal investigator  Grant type：Scientific research funding

  • 歯髄幹細胞移植による胸腺機能の改善を介した免疫調節機序の研究

    Grant number：21K16932  2021 - 2023

    日本学術振興会  科学研究費助成事業  若手研究

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    Grant type：Scientific research funding

  • 胆道閉鎖症患児由来の乳歯幹細胞を用いた病態解析および疾患治療のための基礎研究

    2019.4 - 2021.3

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    Authorship：Principal investigator 

    成体幹細胞が生体の恒常性の維持と組織修復に働く。一方で、成体幹細胞に生じた変異 が疾患を誘発することも知られている。幹細胞は、外因性に受けた障害をエピジェネティ ックな変異として遺伝情報に記憶し、その組織発生や再生・修復の能力が障害され、病態へ 発展することが報告されている。従って、その成体幹細胞の障害記憶を解析することが病 因解明へ繋がると考えられる。本研究では、疾患由来の乳歯幹細胞 stem cells from exfoliated deciduous teeth(SHED)の間葉系幹細胞 mesenchymal stem cells(MSCs)としての障害記憶 力を利用して、胆道閉鎖症の病因解明ならびに自家幹細胞移植治療を目指す研究を行う。

  • 胆道閉鎖症患児由来の乳歯幹細胞を用いた病態解析および疾患治療のための基礎研究

    Grant number：19K18945  2019 - 2020

    日本学術振興会  科学研究費助成事業  若手研究

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    Authorship：Principal investigator  Grant type：Scientific research funding

  • 患者由来乳歯幹細胞を用いた肝疾患病因解析と幹細胞治療

    Grant number：17J03382  2017 - 2018

    日本学術振興会  科学研究費助成事業  基盤研究(C)

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    Grant type：Scientific research funding

  • 患者由来乳歯幹細胞を用いた肝疾患病因解析と幹細胞治療

    Grant number：17J0382  2017 - 2018

    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

  • 分子口腔解剖学（高年次）　D

    2023.12 - 2024.2   Winter quarter

  • 解剖学実習２

    2023.12 - 2024.2   Winter quarter

  • 口腔解剖学４

    2023.12 - 2024.2   Winter quarter

  • 口腔組織学３

    2023.12 - 2024.2   Winter quarter

  • 分子口腔解剖学（低年次）　D

    2023.12 - 2024.2   Winter quarter

  • 分子口腔解剖学（コア）　D

    2023.12 - 2024.2   Winter quarter

  • 分子口腔解剖学（高年次）　C

    2023.10 - 2023.12   Fall quarter

  • 解剖学実習１

    2023.10 - 2023.12   Fall quarter

  • 口腔解剖学３

    2023.10 - 2023.12   Fall quarter

  • 口腔組織学２

    2023.10 - 2023.12   Fall quarter

  • 分子口腔解剖学（低年次）　C

    2023.10 - 2023.12   Fall quarter

  • 分子口腔解剖学（コア）　C

    2023.10 - 2023.12   Fall quarter

  • 分子口腔解剖学（高年次）　B

    2023.6 - 2023.8   Summer quarter

  • 口腔組織学１

    2023.6 - 2023.8   Summer quarter

  • 解剖学２

    2023.6 - 2023.8   Summer quarter

  • 口腔解剖学２

    2023.6 - 2023.8   Summer quarter

  • 分子口腔解剖学（低年次）　B

    2023.6 - 2023.8   Summer quarter

  • 分子口腔解剖学（コア）　B

    2023.6 - 2023.8   Summer quarter

  • 分子口腔解剖学（高年次）　A

    2023.4 - 2023.6   Spring quarter

  • 発生学

    2023.4 - 2023.6   Spring quarter

  • 解剖学１

    2023.4 - 2023.6   Spring quarter

  • 口腔解剖学１

    2023.4 - 2023.6   Spring quarter

  • 分子口腔解剖学（低年次）　A

    2023.4 - 2023.6   Spring quarter

  • 分子口腔解剖学（コア）　A

    2023.4 - 2023.6   Spring quarter

  • 解剖学実習２

    2022.12 - 2023.2   Winter quarter

  • 分子口腔解剖学（高年次）　D

    2022.12 - 2023.2   Winter quarter

  • 分子口腔解剖学（コア）　D

    2022.12 - 2023.2   Winter quarter

  • 分子口腔解剖学（低年次）　D

    2022.12 - 2023.2   Winter quarter

  • 口腔組織学３

    2022.12 - 2023.2   Winter quarter

  • 口腔解剖学４

    2022.12 - 2023.2   Winter quarter

  • 解剖学実習１

    2022.10 - 2022.12   Fall quarter

  • 分子口腔解剖学（高年次）　C

    2022.10 - 2022.12   Fall quarter

  • 分子口腔解剖学（コア）　C

    2022.10 - 2022.12   Fall quarter

  • 分子口腔解剖学（低年次）　C

    2022.10 - 2022.12   Fall quarter

  • 口腔組織学２

    2022.10 - 2022.12   Fall quarter

  • 口腔解剖学３

    2022.10 - 2022.12   Fall quarter

  • 口腔組織学１

    2022.6 - 2022.8   Summer quarter

  • 分子口腔解剖学（高年次）　B

    2022.6 - 2022.8   Summer quarter

  • 分子口腔解剖学（コア）　B

    2022.6 - 2022.8   Summer quarter

  • 分子口腔解剖学（低年次）　B

    2022.6 - 2022.8   Summer quarter

  • 口腔解剖学２

    2022.6 - 2022.8   Summer quarter

  • 解剖学２

    2022.6 - 2022.8   Summer quarter

  • 発生学

    2022.4 - 2022.6   Spring quarter

  • 分子口腔解剖学（高年次）　A

    2022.4 - 2022.6   Spring quarter

  • 分子口腔解剖学（コア）　A

    2022.4 - 2022.6   Spring quarter

  • 分子口腔解剖学（低年次）　A

    2022.4 - 2022.6   Spring quarter

  • 口腔解剖学１

    2022.4 - 2022.6   Spring quarter

  • 解剖学１

    2022.4 - 2022.6   Spring quarter

  • 分子口腔解剖学（高年次）　D

    2021.12 - 2022.2   Winter quarter

  • 分子口腔解剖学（低年次）　D

    2021.12 - 2022.2   Winter quarter

  • 分子口腔解剖学（コア）　D

    2021.12 - 2022.2   Winter quarter

  • 口腔組織学２

    2021.10 - 2022.3   Second semester

  • 分子口腔解剖学（高年次）　C

    2021.10 - 2021.12   Fall quarter

  • 分子口腔解剖学（低年次）　C

    2021.10 - 2021.12   Fall quarter

  • 分子口腔解剖学（コア）　C

    2021.10 - 2021.12   Fall quarter

  • 分子口腔解剖学（高年次）　B

    2021.6 - 2021.8   Summer quarter

  • 分子口腔解剖学（低年次）　B

    2021.6 - 2021.8   Summer quarter

  • 分子口腔解剖学（コア）　B

    2021.6 - 2021.8   Summer quarter

  • 口腔解剖学

    2021.4 - 2022.3   Full year

  • 解剖学

    2021.4 - 2022.3   Full year

  • 口腔組織学１

    2021.4 - 2021.9   First semester

  • 発生学

    2021.4 - 2021.9   First semester

  • 分子口腔解剖学（高年次）　A

    2021.4 - 2021.6   Spring quarter

  • 分子口腔解剖学（低年次）　A

    2021.4 - 2021.6   Spring quarter

  • 分子口腔解剖学（コア）　A

    2021.4 - 2021.6   Spring quarter

  • 口腔組織学II

    2020.10 - 2021.3   Second semester

  • 口腔解剖学

    2020.4 - 2021.3   Full year

  • 解剖学

    2020.4 - 2021.3   Full year

  • 発生学

    2020.4 - 2020.9   First semester

  • 口腔組織学1

    2020.4 - 2020.9   First semester

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FD Participation

  • 2019.4   Role：Participation   Title：平成３１年度 第１回全学ＦＤ（新任教員の研修）

    Organizer：University-wide

Other educational activity and Special note

  • 2022  Special Affairs 

  • 2021  Special Affairs 

  • 2020  Special Affairs 

  • 2019  Special Affairs