Updated on 2024/10/03

Information

 

写真a

 
KATO HIROKI
 
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
Profile
「口腔組織由来細胞を用いた先天性疾患に関する研究」：先天性疾患(ダウン症、先天性代謝疾患、自閉症、口唇裂口蓋裂等)の多くは、未だ決定的な治療法が開発されていません。私は先天性疾患の患者の口腔組織から幹細胞を調製し、これを活用した病態解析と新規治療法の開発、さらに再生医療のための細胞源として口腔組織由来幹細胞の活用を目標にして研究を行っています。　　　　　　　　　　 　　　「オルガネラの生合成および機能調節についての研究」：高等生物の細胞内には，膜で囲まれたそれぞれ異なる機能を持つ小区画が存在しています。これら小区画はオルガネラと呼ばれ，そこには特有のタンパク質が存在しており生命に不可欠な生化学反応を行っています。私は，このオルガネラの生合成および機能調節について，特にミトコンドリアに焦点を当てに研究を行っています。
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Degree

  • Doctor of Science

Research History

  • Universität Tübingen, 東京医科大学   

Research Interests・Research Keywords

  • Research theme： 　

    Keyword： 　

    Research period： 2014.11 - Present

  • Research theme： Analysis of mitochondrial dynamics

    Keyword： mitochondria, membrane dynamics

    Research period： 2014.5 - Present

Awards

  • 第61回宇部興産学術振興財団学術奨励賞

    2021.4   公益財団法人宇部興産学術振興財団  

  • 第61回日本小児神経学会奨励賞

    2019.5   日本小児神経学会  

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, and Takayoshi Yamaza

    Journal of Cell Science   2024.9

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

    DOI： https://doi.org/10.1242/jcs.261732

  • Dopamine-related oxidative stress and mitochondrial dysfunction in dopaminergic neurons differentiated from deciduous teeth-derived stem cells of children with Down syndrome Reviewed

    Xiao Sun, Hiroki Kato, Hiroshi Sato, Xu Han, Yuta Hirofuji, Takahiro A. Kato, Yasunari Sakai, Shouichi Ohga, Satoshi Fukumoto, Keiji Masuda

    FASEB BioAdvances   2022.4

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    Authorship：Lead author   Language：Japanese   Publishing type：Research paper (scientific journal)  

    DOI： 10.1096/fba.2021-00086

  • Accelerated osteoblastic differentiation in patient-derived dental pulp stem cells carrying a gain-of-function mutation of TRPV4 associated with metatropic dysplasia Reviewed

    Xu Han, Hiroki Kato, Hiroshi Sato, Yuta Hirofuji, Satoshi Fukumoto, Keiji Masuda

    Biochemical and Biophysical Research Communications   523 ( 4 )   841 - 846   2020.3

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

    Metatropic dysplasia (MD) is a congenital skeletal dysplasia characterized by severe platyspondyly and dumbbell-like long-bone deformities. These skeletal phenotypes are predominantly caused by autosomal dominant gain-of-function (GOF) mutations in transient receptor potential vanilloid 4 (TRPV4), which encodes a nonselective Ca2+-permeable cation channel. Previous studies have shown that constitutive TRPV4 channel activation leads to irregular chondrogenic proliferation and differentiation, and thus to the disorganized endochondral ossification seen in MD. Therefore, the present study investigated the role of TRPV4 in osteoblast differentiation and MD pathogenesis. Specifically, the behavior of osteoblasts differentiated from patient-derived dental pulp stem cells carrying a heterozygous single base TRPV4 mutation, c.1855C > T (p.L619F) was compared to that of osteoblasts differentiated from isogenic control cells (in which the mutation was corrected using the CRISPR/Cas9 system). The mutant osteoblasts exhibited enhanced calcification (indicated by intense Alizarin Red S staining), increased intracellular Ca2+ levels, strongly upregulated runt-related transcription factor 2 and osteocalcin expression, and increased expression and nuclear translocation of nuclear factor-activated T cell c1 (NFATc1) compared to control cells. These results suggest that the analyzed TRPV4 GOF mutation disrupts osteoblastic differentiation and induces MD-associated disorganized endochondral ossification by increasing Ca2+/NFATc1 pathway activity. Thus, inhibiting the NFATc1 pathway may be a promising potential therapeutic strategy to attenuate skeletal deformities in MD.

    DOI： 10.1016/j.bbrc.2019.12.123

  • Novel gain-of-function mutation of TRPV4 associated with accelerated chondrogenic differentiation of dental pulp stem cells derived from a patient with metatropic dysplasia Reviewed

    Kentaro Nonaka, Xu Han, Hiroki Kato, Hiroshi Sato, Haruyoshi Yamaza, Yuta Hirofuji, Keiji Masuda

    Biochemistry and Biophysics Reports   19   2019.9

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    Authorship：Corresponding author   Language：English   Publishing type：Research paper (scientific journal)  

    Metatropic dysplasia is a congenital skeletal dysplasia characterized by severe platyspondyly, dumbbell-like deformity of long tubular bones, and progressive kyphoscoliosis with growth. It is caused by mutations in the gene TRPV4, encoding the transient receptor potential vanilloid 4, which acts as a calcium channel. Many heterozygous single base mutations of this gene have been associated with the disorder, showing autosomal dominant inheritance. Although abnormal endochondral ossification has been observed by histological examination of bone in a patient with lethal metatropic dysplasia, the etiology of the disorder remains largely unresolved. As dental pulp stem cells (DPSCs) are mesenchymal stem cells that differentiate into bone lineage cells, DPSCs derived from patients with congenital skeletal dysplasia might be useful as a disease-specific cellular model for etiological investigation. The purpose of this study was to clarify the pathological association between TRPV4 mutation and chondrocyte differentiation by analyzing DPSCs from a patient with non-lethal metatropic dysplasia. We identified a novel heterozygous single base mutation, c.1855C>T in TRPV4. This was predicted to be a missense mutation, p.L619F, in putative transmembrane segment 5. The mutation was repaired by CRISPR/Cas9 system to obtain isogenic control DPSCs for further analysis. The expression of stem cell markers and fibroblast-like morphology were comparable between patient-derived mutant and control DPSCs, although expression of TRPV4 was lower in mutant DPSCs than control DPSCs. Despite the lower TRPV4 expression in mutant DPSCs, the intracellular Ca2+ level was comparable at the basal level between mutant and control DPSCs, while its level was markedly higher following stimulation with 4α-phorbol 12,13-didecanoate (4αPDD), a specific agonist for TRPV4, in mutant DPSCs than in control DPSCs. In the presence of 4αPDD, we observed accelerated early chondrocyte differentiation and upregulated mRNA expression of SRY-box 9 (SOX9) in mutant DPSCs. Our findings suggested that the novel missense mutation c.1855C>T of TRPV4 was a gain-of-function mutation leading to enhanced intracellular Ca2+ level, which was associated with accelerated chondrocyte differentiation and SOX9 upregulation. Our results also suggest that patient-derived DPSCs can be a useful disease-specific cellular model for elucidating the pathological mechanism of metatropic dysplasia.

    DOI： 10.1016/j.bbrep.2019.100648

  • Osteoblastic differentiation improved by bezafibrate-induced mitochondrial biogenesis in deciduous tooth-derived pulp stem cells from a child with Leigh syndrome Reviewed

    Xu Han, Kentaro Nonaka, Hiroki Kato, Haruyoshi Yamaza, Hiroshi Sato, Takashi Kifune, Yuta Hirofuji, Keiji Masuda

    Biochemistry and Biophysics Reports   17   32 - 37   2019.3

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    Authorship：Corresponding author   Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1016/j.bbrep.2018.11.003

  • Positive effect of exogenous brain-derived neurotrophic factor on impaired neurite development and mitochondrial function in dopaminergic neurons derived from dental pulp stem cells from children with attention deficit hyperactivity disorder Reviewed

    Huong Thi Nguyen Nguyen, Hiroki Kato, Hiroshi Sato, Haruyoshi Yamaza, Yasunari Sakai, Shoichi Ohga, Kazuaki Nonaka, Keiji Masuda

    Biochemical and Biophysical Research Communications   2019.1

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    Attention deficit hyperactivity disorder (ADHD) is one of the most common neurodevelopmental disorders and is characterized by impaired attention, hyperactivity, and impulsivity. While multiple etiologies are implicated in ADHD, its underlying mechanism(s) remain unclear. Although previous studies have suggested dysregulation of dopaminergic signals, mitochondria, and brain-derived neurotrophic factor (BDNF) in ADHD, few studies have reported these associations directly. Stem cells from human exfoliated deciduous teeth (SHED) can efficiently differentiate into dopaminergic neurons (DNs) and are thus a useful disease-specific cellular model for the study of neurodevelopmental disorders associated with DN dysfunction. This study aimed to elucidate the relationships between DNs, mitochondria, and BDNF in ADHD by analyzing DNs differentiated from SHED obtained from three boys with ADHD and comparing them to those from three typically developing boys. In the absence of exogenous BDNF in the cell culture media, DNs derived from boys with ADHD (ADHD-DNs) exhibited impaired neurite outgrowth and branching, decreased mitochondrial mass in neurites, and abnormal intracellular ATP levels. In addition, BDNF mRNA was significantly decreased in ADHD-DNs. Supplementation with BDNF, however, significantly improved neurite development and mitochondrial function in ADHD-DNs. These results suggest that ADHD-DNs may have impaired neurite development and mitochondrial function associated with insufficient production of BDNF, which may be improved by exogenous BDNF supplementation. Findings such as these, from patient-derived SHED, may contribute to the future development of treatment strategies for aberrant dopaminergic signaling, mitochondrial functioning, and BDNF levels implicated in ADHD pathogenesis.

    DOI： 10.1016/j.bbrc.2019.04.084

  • Folic acid-mediated mitochondrial activation for protection against oxidative stress in human dental pulp stem cells derived from deciduous teeth Reviewed

    Yu Zhang, Hiroki Kato, Hiroshi Sato, Haruyoshi Yamaza, Yuta Hirofuji, Xu Han, Keiji Masuda, Kazuaki Nonaka

    Biochemical and biophysical research communications   2019.1

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    DOI： 10.1016/j.bbrc.2018.11.169

  • Impaired neurite development associated with mitochondrial dysfunction in dopaminergic neurons differentiated from exfoliated deciduous tooth-derived pulp stem cells of children with autism spectrum disorder Reviewed

    Huong Thi Nguyen Nguyen, Hiroki Kato, Keiji Masuda, Haruyoshi Yamaza, Yuta Hirofuji, Hiroshi Sato, Thanh Thi Mai Pham, Fumiko Takayama, Yasunari Sakai, Shoichi Ohga, Tomoaki Taguchi, Kazuaki Nonaka

    Biochemistry and Biophysics Reports   16   24 - 31   2018.12

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    Authorship：Lead author,　Corresponding author   Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1016/j.bbrep.2018.09.004

  • Altered development of dopaminergic neurons differentiated from stem cells from human exfoliated deciduous teeth of a patient with Down syndrome Reviewed

    Thanh Thi Mai Pham, Hiroki Kato, Haruyoshi Yamaza, Keiji Masuda, Yuta Hirofuji, Hiroshi Sato, Huong Thi Nguyen Nguyen, Xu Han, Yu Zhang, Tomoaki Taguchi, Kazuaki Nonaka

    BMC Neurology   18 ( 1 )   2018.8

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    Authorship：Corresponding author   Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1186/s12883-018-1140-2

  • Mitochondrial dysfunction in dopaminergic neurons differentiated from exfoliated deciduous tooth-derived pulp stem cells of a child with Rett syndrome Reviewed

    Saki Hirofuji, Yuta Hirofuji, Hiroki Kato, Keiji Masuda, Haruyoshi Yamaza, Hiroshi Sato, Fumiko Takayama, Michiko Torio, Yasunari Sakai, Shoichi Ohga, Tomoaki Taguchi, Kazuaki Nonaka

    Biochemical and Biophysical Research Communications   498 ( 4 )   898 - 904   2018.4

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    DOI： 10.1016/j.bbrc.2018.03.077

  • Accelerated dentinogenesis by inhibiting the mitochondrial fission factor, dynamin related protein 1 Reviewed

    Yumiko I. Matsuishi, Hiroki Kato, Keiji Masuda, Haruyoshi Yamaza, Yuta Hirofuji, Hiroshi Sato, Hiroko Wada, Tamotsu Kiyoshima, Kazuaki Nonaka

    Biochemical and Biophysical Research Communications   495 ( 2 )   1655 - 1660   2018.1

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

    DOI： 10.1016/j.bbrc.2017.12.026

  • Direct effects of mitochondrial dysfunction on poor bone health in Leigh syndrome Reviewed

    Hiroki Kato, Xu Han, Haruyoshi Yamaza, Keiji Masuda, Yuta Hirofuji, Hiroshi Sato, Thanh Thi Mai Pham, Tomoaki Taguchi, Kazuaki Nonaka

    Biochemical and Biophysical Research Communications   493 ( 1 )   207 - 212   2017.11

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    Authorship：Lead author,　Corresponding author   Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1016/j.bbrc.2017.09.045

  • Mitochondria regulate the differentiation of stem cells from human exfoliated deciduous teeth Reviewed

    Hiroki Kato, Thanh Thi Mai Pham, Haruyoshi Yamaza, Keiji Masuda, Yuta Hirofuji, Xu Han, Hiroshi Sato, Tomoaki Taguchi, Kazuaki Nonaka

    Cell Structure and Function   42 ( 2 )   105 - 116   2017.5

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    Authorship：Lead author,　Corresponding author   Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1247/csf.17012

    Repository Public URL： https://hdl.handle.net/2324/7174333

  • Tom70 Is Essential for PINK1 Import into Mitochondria Reviewed

    Hiroki Kato, Qiping Lu, Doron Rapaport, Vera Kozjak-Pavlovic

    PLoS One   8 ( 3 )   2013.3

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    Authorship：Lead author,　Corresponding author   Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1371/journal.pone.0058435

  • Identification of Tom5 and Tom6 in the preprotein translocase complex of human mitochondrial outer membrane Reviewed

    Hiroki Kato, Katsuyoshi Mihara

    Biochemical and Biophysical Research Communications   369 ( 3 )   958 - 963   2008.5

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

    DOI： 10.1016/j.bbrc.2008.02.150

  • Ubiquitin-proteasome-dependent degradation of mammalian ER stearoyl-CoA desaturase Reviewed

    Hiroki Kato, Kenjiro Sakaki, Katsuyoshi Mihara

    Journal of Cell Science   119 ( 11 )   2342 - 2353   2006.6

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    DOI： 10.1242/jcs.02951

  • Gnao1 is a molecular switch that regulates the Rho signaling pathway in differentiating neurons Reviewed

    Ryoji Taira;Satoshi Akamine;Sayaka Okuzono;Fumihiko Fujii;Eriko Hatai;Kousuke Yonemoto;Ryuichi Takemoto;Hiroki Kato;Keiji Masuda;Takahiro A. Kato;Ryutaro Kira;Keita Tsujimura;Kenichiro Yamamura;Norio Ozaki;Shouichi Ohga;Yasunari Sakai

    Scientific Reports   14 ( 1 )   2024.7

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

    DOI： 10.1038/s41598-024-68062-x

  • An N‐terminal and ankyrin repeat domain interactome of Shank3 identifies the protein complex with the splicing regulator Nono in mice Reviewed

    Sayaka Okuzono;Fumihiko Fujii;Daiki Setoyama;Ryoji Taira;Yohei Shinmyo;Hiroki Kato;Keiji Masuda;Kousuke Yonemoto;Satoshi Akamine;Yuki Matsushita;Yoshitomo Motomura;Takeshi Sakurai;Hiroshi Kawasaki;Kihoon Han;Takahiro A. Kato;Hiroyuki Torisu;Dongchon Kang;Yusaku Nakabeppu;Shouichi Ohga;Yasunari Sakai

    Genes to Cells   2024.7

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  • ATP1A3 regulates protein synthesis for mitochondrial stability under heat stress. Reviewed

    Fumihiko Fujii;Hikaru Kanemasa;Sayaka Okuzono;Daiki Setoyama;Ryoji Taira;Kousuke Yonemoto;Yoshitomo Motomura;Hiroki Kato;Keiji Masuda;Takahiro A Kato;Shouichi Ohga;Yasunari Sakai

    Disease models & mechanisms   2024.5

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

    Zakaria, F., Sonoda, S., Kato, H., Ma, L., Uehara, N., Kyumoto-Nakamura, Y., Sharifa, M., Yu, L., Dai, L., Yamauchi-Tomoda, E., Aijima, R., Yamaza, H., Nishimura, F., Yamaza, T.

    Sci Rep.   2024.3

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

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

    Arch Biochem Biophys.   2023.11

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  • TRPV4-mediated Ca2+ deregulation causes mitochondrial dysfunction via the AKT/α-synuclein pathway in dopaminergic neurons. Reviewed International journal

    Sun, X., Kong, J., Dong, S., Kato, H., Sato, H., Hirofuji, Y., Ito, Y., Wang, L., Kato, T.A., Torio, M., Sakai, Y., Ohga, S., Fukumoto, S., Masuda, K.

    FASEB Bioadv.   2023.10

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  • Effects of melatonin on dopaminergic neuron development via IP3-mediated mitochondrial Ca2+ regulation in autism spectrum disorder. Reviewed International journal

    Dong, S., Kifune, T., Kato, H., Wang, L., Kong, J., Hirofuji, Y., Sun, X., Sato, H., Ito, Y., Kato, T.A., Sakai, Y., Ohga, S., Fukumoto, S., Masuda, K.

    Biochem Biophys Res Commun.   2023.9

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  • Mitochondrial Calcium-Triggered Oxidative Stress and Developmental Defects in Dopaminergic Neurons Differentiated from Deciduous Teeth-Derived Dental Pulp Stem Cells with MFF Insufficiency Reviewed International journal

    Sun, Xiao; Dong, Shuangshan; Kato, Hiroki; Kong, Jun; Ito, Yosuke; Hirofuji, Yuta; Sato, Hiroshi; Kato, Takahiro A.; Sakai, Yasunari; Ohga, Shouichi; Fukumoto, Satoshi; Masuda, Keiji

    ANTIOXIDANTS   11 ( 7 )   2022.7

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

    DOI： 10.3390/antiox11071361

  • Stem cells from human exfoliated deciduous teeth attenuate mechanical allodynia in mice through distinct from the siglec-9/MCP-1-mediated tissue-repairing mechanism Invited Reviewed International journal

    Hayashi, Yoshinori; Kato, Hiroki; Nonaka, Kazuaki; Nakanishi, Hiroshi

    SCIENTIFIC REPORTS   11 ( 1 )   2021.10

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

    DOI： 10.1038/s41598-021-99585-2

  • Impaired neurite development and mitochondrial dysfunction associated with calcium accumulation in dopaminergic neurons differentiated from the dental pulp stem cells of a patient with metatropic dysplasia Reviewed International journal

    Xiao Sun, Hiroki Kato, Hiroshi Sato, Michiko Torio, Xu Han, Yu Zhang, Yuta Hirofuji, Takahiro A Kato, Yasunari Sakai, Shouichi Ohga, Satoshi Fukumoto, Keiji Masuda

    Biochemistry and Biophysics Reports   ( 26 )   100968   2021.7

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    Transient receptor potential vanilloid member 4 (TRPV4) is a Ca2+ permeable nonselective cation channel, and mutations in the TRPV4 gene cause congenital skeletal dysplasias and peripheral neuropathies. Although TRPV4 is widely expressed in the brain, few studies have assessed the pathogenesis of TRPV4 mutations in the brain. We aimed to elucidate the pathological associations between a specific TRPV4 mutation and neurodevelopmental defects using dopaminergic neurons (DNs) differentiated from dental pulp stem cells (DPSCs). DPSCs were isolated from a patient with metatropic dysplasia and multiple neuropsychiatric symptoms caused by a gain-of-function TRPV4 mutation, c.1855C>T (p.L619F). The mutation was corrected by CRISPR/Cas9 to obtain isogenic control DPSCs. Mutant DPSCs differentiated into DNs without undergoing apoptosis; however, neurite development was significantly impaired in mutant vs. control DNs. Mutant DNs also showed accumulation of mitochondrial Ca2+ and reactive oxygen species, low adenosine triphosphate levels despite a high mitochondrial membrane potential, and lower peroxisome proliferator-activated receptor gamma coactivator 1-alpha expression and mitochondrial content. These results suggested that the persistent Ca2+ entry through the constitutively activated TRPV4 might perturb the adaptive coordination of multiple mitochondrial functions, including oxidative phosphorylation, redox control, and biogenesis, required for dopaminergic circuit development in the brain. Thus, certain mutations in TRPV4 that are associated with skeletal dysplasia might have pathogenic effects on brain development, and mitochondria might be a potential therapeutic target to alleviate the neuropsychiatric symptoms of TRPV4-related diseases.

    DOI： 10.1016/j.bbrep.2021.100968.

  • Targeting of Deciduous Tooth Pulp Stem Cell-Derived Extracellular Vesicles on Telomerase-Mediated Stem Cell Niche and Immune Regulation in Systemic Lupus Erythematosus Reviewed International journal

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

    JOURNAL OF IMMUNOLOGY   206 ( 12 )   3053 - 3063   2021.6

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

    DOI： 10.4049/jimmunol.2001312

  • Dental Pulp-Derived Mesenchymal Stem Cells for Modeling Genetic Disorders Invited Reviewed International journal

    Masuda, Keiji; Han, Xu; Kato, Hiroki; Sato, Hiroshi; Zhang, Yu; Sun, Xiao; Hirofuji, Yuta; Yamaza, Haruyoshi; Yamada, Aya; Fukumoto, Satoshi

    INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES   22 ( 5 )   2021.3

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    A subpopulation of mesenchymal stem cells, developmentally derived from multipotent neural crest cells that form multiple facial tissues, resides within the dental pulp of human teeth. These stem cells show high proliferative capacity in vitro and are multipotent, including adipogenic, myogenic, osteogenic, chondrogenic, and neurogenic potential. Teeth containing viable cells are harvested via minimally invasive procedures, based on various clinical diagnoses, but then usually discarded as medical waste, indicating the relatively low ethical considerations to reuse these cells for medical applications. Previous studies have demonstrated that stem cells derived from healthy subjects are an excellent source for cell-based medicine, tissue regeneration, and bioengineering. Furthermore, stem cells donated by patients affected by genetic disorders can serve as in vitro models of disease-specific genetic variants, indicating additional applications of these stem cells with high plasticity. This review discusses the benefits, limitations, and perspectives of patient-derived dental pulp stem cells as alternatives that may complement other excellent, yet incomplete stem cell models, such as induced pluripotent stem cells, together with our recent data.

    DOI： 10.3390/ijms22052269

  • GNAO1 organizes the cytoskeletal remodeling and firing of developing neurons Reviewed International journal

    Akamine, Satoshi; Okuzono, Sayaka; Yamamoto, Hiroyuki; Setoyama, Daiki; Sagata, Noriaki; Ohgidani, Masahiro; Kato, Takahiro A.; Ishitani, Tohru; Kato, Hiroki; Masuda, Keiji; Matsushita, Yuki; Ono, Hiroaki; Ishizaki, Yoshito; Sanefuji, Masafumi; Saitsu, Hirotomo; Matsumoto, Naomichi; Kang, Dongchon; Kanba, Shigenobu; Nakabeppu, Yusaku; Sakai, Yasunari; Ohga, Shouichi

    FASEB JOURNAL   34 ( 12 )   16601 - 16621   2020.12

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    Developmental and epileptic encephalopathy (DEE) represents a group of neurodevelopmental disorders characterized by infantile-onset intractable seizures and unfavorable prognosis of psychomotor development. To date, hundreds of genes have been linked to the onset of DEE. GNAO1 is a DEE-associated gene encoding the alpha-O1 subunit of guanine nucleotide-binding protein (GαO ). Despite the increasing number of reported children with GNAO1 encephalopathy, the molecular mechanisms underlying their neurodevelopmental phenotypes remain elusive. We herein present that co-immunoprecipitation and mass spectrometry analyses identified another DEE-associated protein, SPTAN1, as an interacting partner of GαO . Silencing of endogenous Gnao1 attenuated the neurite outgrowth and calcium-dependent signaling. Inactivation of GNAO1 in human-induced pluripotent stem cells gave rise to anomalous brain organoids that only weakly expressed SPTAN1 and Ankyrin-G. Furthermore, GNAO1-deficient organoids failed to conduct synchronized firing to adjacent neurons. These data indicate that GαO and other DEE-associated proteins organize the cytoskeletal remodeling and functional polarity of neurons in the developing brain.

    DOI： 10.1096/fj.202001113R

  • Forskolin rapidly enhances neuron-like morphological change of directly induced-neuronal cells from neurofibromatosis type 1 patients Reviewed International journal

    Noriaki Sagata, Shin‐ichi Kano, Masahiro Ohgidani, Shogo Inamine, Yasunari Sakai, Hiroki Kato, Keiji Masuda, Takeshi Nakahara, Makiko Nakahara‐Kido, Shouichi Ohga, Masutaka Furue, Akira Sawa, Shigenobu Kanba, Takahiro A. Kato

    Neuropsychopharmacol Rep.   2020.10

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    Aim: Neurofibromatosis type 1 (NF1) is a multifaceted disease, and frequently comorbid with neurodevelopmental disorders such as autism spectrum disorder (ASD) and learning disorder. Dysfunction of adenylyl cyclase (AC) is one of the candidate pathways in abnormal development of neuronal cells in the brain of NF1 patients, while its dynamic abnormalities have not been observed. Direct conversion technology can generate induced-neuronal (iN) cells directly from human fibroblasts within 2 weeks. Just recently, we have revealed that forskolin, an AC activator, rescues the gene expression pattern of iN cells derived from NF1 patients (NF1-iN cells). In this microreport, we show the dynamic effect of forskolin on NF1-iN cells.

    Methods: iN cells derived from healthy control (HC-iN cells) and NF1-iN cells were treated with forskolin (final concentration 10 μM), respectively. Morphological changes of iN cells were captured by inverted microscope with CCD camera every 2 minutes for 90 minutes.

    Results: Prior to forskolin treatment, neuron-like spherical-form cells were observed in HC-iN cells, but most NF1-iN cells were not spherical-form but flatform. Only 20 minutes after forskolin treatment, the morphology of the iN cells were dramatically changed from flatform to spherical form, especially in NF1-iN cells.

    Conclusion: The present pilot data indicate that forskolin or AC activators may have therapeutic effects on the growth of neuronal cells in NF1 patients. Further translational research should be conducted to validate our pilot findings for future drug development of ASD.

  • 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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    Background: Systemic transplantation of stem cells from human exfoliated deciduous teeth (SHED) recovers bone loss in animal models of osteoporosis; however, the mechanisms underlying this remain unclear. Here, we hypothesized that trophic factors within SHED-releasing extracellular vesicles (SHED-EVs) rescue osteoporotic phenotype. Methods: EVs were isolated from culture supernatant of SHED. SHED-EVs were treated with or without ribonuclease and systemically administrated into ovariectomized mice, followed by the function of recipient bone marrow mesenchymal stem cells (BMMSCs) including telomerase activity, osteoblast differentiation, and sepmaphorine-3A (SEMA3A) secretion. Subsequently, human BMMSCs were stimulated by SHED-EVs with or without ribonuclease treatment, and then human BMMSCs were examined regarding the function of telomerase activity, osteoblast differentiation, and SEMA3A secretion. Furthermore, SHED-EV-treated human BMMSCs were subcutaneously transplanted into the dorsal skin of immunocompromised mice with hydroxyapatite tricalcium phosphate (HA/TCP) careers and analyzed the de novo bone-forming ability. Results: We revealed that systemic SHED-EV-infusion recovered bone volume in ovariectomized mice and improved the function of recipient BMMSCs by rescuing the mRNA levels of Tert and telomerase activity, osteoblast differentiation, and SEMA3A secretion. Ribonuclease treatment depleted RNAs, including microRNAs, within SHED-EVs, and these RNA-depleted SHED-EVs attenuated SHED-EV-rescued function of recipient BMMSCs in the ovariectomized mice. These findings were supported by in vitro assays using human BMMSCs incubated with SHED-EVs. Conclusion: Collectively, our findings suggest that SHED-secreted RNAs, such as microRNAs, play a crucial role in treating postmenopausal osteoporosis by targeting the telomerase activity of recipient BMMSCs.

    DOI： 10.1186/s13287-020-01818-0

  • Engineering of Systematic Elimination of a Targeted Chromosome in Human Cells Reviewed

    Hiroshi Sato, Hiroki Kato, Haruyoshi Yamaza, Keiji Masuda, Huong Thi Nguyen Nguyen, Thanh Thi Mai Pham, Xu Han, Yuta Hirofuji, Kazuaki Nonaka

    BioMed Research International   2017   2017.1

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

    DOI： 10.1155/2017/6037159

  • PKA Regulates PINK1 Stability and Parkin Recruitment to Damaged Mitochondria through Phosphorylation of MIC60 Reviewed

    Shiori Akabane, Midori Uno, Naoki Tani, Shunta Shimazaki, Natsumi Ebara, Hiroki Kato, Hidetaka Kosako, Toshihiko Oka

    Molecular Cell   62 ( 3 )   371 - 384   2016.5

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

    DOI： 10.1016/j.molcel.2016.03.037

  • Mitochondrial physiology and cerebrospinal protection

    Morika Suzuki, Hiroki Kato, Naomi Hachiya

    Neuroanesthesia and Cerebrospinal Protection   63 - 70   2015.8

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    Language：English  

    DOI： 10.1007/978-4-431-54490-6_6

  • Propofol prevents mitochondrial fragmentation Reviewed

    Morika Suzuki, Hiroyuki Uchino, Hiroki Kato

    Journal of Tokyo Medical University   73 ( 3 )   268 - 275   2015.1

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

  • Mitochondrial proteolytic stress induced by loss of mortalin function is rescued by Parkin and PINK1 Reviewed

    L. F. Burbulla, J. C. Fitzgerald, K. Stegen, J. Westermeier, A. K. Thost, Hiroki Kato, D. Mokranjac, J. Sauerwald, L. M. Martins, D. Woitalla, D. Rapaport, O. Riess, T. Proikas-Cezanne, T. M. Rasse, R. Krüger

    Cell Death and Disease   5 ( 4 )   2014.1

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

    DOI： 10.1038/cddis.2014.103

  • 14-3-3 proteins sequester a pool of soluble TRIM32 ubiquitin ligase to repress autoubiquitylation and cytoplasmic body formation Reviewed

    Tohru Ichimura, Masato Taoka, Ikuo Shoji, Hiroki Kato, Tomonobu Sato, Shigetsugu Hatakeyama, Toshiaki Isobe, Naomi Hachiya

    Journal of Cell Science   126 ( 9 )   2014 - 2026   2013.5

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

    DOI： 10.1242/jcs.122069

  • Dissecting the role of the mitochondrial chaperone mortalin in Parkinson's disease Functional impact of disease-related variants on mitochondrial homeostasis Reviewed

    Lena F. Burbulla, Carina Schelling, Hiroki Kato, Doron Rapaport, Dirk Woitalla, Carola Schiesling, Claudia Schulte, Manu Sharma, Thomas Illig, Peter Bauer, Stephan Jung, Alfred Nordheim, Ludger Schöls, Olaf Riess, Rejko Krüger

    Human Molecular Genetics   19 ( 22 )   4437 - 4452   2010.11

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

    DOI： 10.1093/hmg/ddq370

  • Proteins of nucleotide and base excision repair pathways interact in mitochondria to protect from loss of subcutaneous fat, a hallmark of aging Reviewed

    York Kamenisch, Maria Fousteri, Jennifer Knoch, Anna Katharina Von Thaler, Birgit Fehrenbacher, Hiroki Kato, Thomas Becker, Martijn E T Dollé, Raoul Kuiper, Marc Majora, Martin Schaller, Gijsbertus T J Van Der Horst, Harry Van Steeg, Martin Röcken, Doron Rapaport, Jean Krutmann, Leon H. Mullenders, Mark Berneburg

    Journal of Experimental Medicine   207 ( 2 )   379 - 390   2010.2

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

    DOI： 10.1084/jem.20091834

  • Mitochondrial fission factor Drp1 is essential for embryonic development and synapse formation in mice Reviewed

    Naotada Ishihara, Masatoshi Nomura, Akihiro Jofuku, Hiroki Kato, Satoshi Suzuki, Keiji Masuda, Hidenori Otera, Yae Nakanishi, Ikuya Nonaka, Yu Ichi Goto, Naoko Taguchi, Hidetaka Morinaga, Maki Maeda, Ryoichi Takayanagi, Sadaki Yokota, Katsuyoshi Mihara

    Nature Cell Biology   11 ( 8 )   958 - 966   2009.7

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

    DOI： 10.1038/ncb1907

  • Identification of a novel protein MICS1 that is involved in maintenance of mitochondrial morphology and apoptotic release of cytochrome c Reviewed

    Toshihiko Oka, Tomoko Sayano, Shoko Tamai, Sadaki Yokota, Hiroki Kato, Gen Fujii, Katsuyoshi Mihara

    Molecular Biology of the Cell   19 ( 6 )   2597 - 2608   2008.6

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

    DOI： 10.1091/mbc.E07-12-1205

  • A novel insertion pathway of mitochondrial outer membrane proteins with multiple transmembrane segments Reviewed

    Hidenori Otera, Yohsuke Taira, Chika Horie, Yurina Suzuki, Hiroyuki Suzuki, Kiyoko Setoguchi, Hiroki Kato, Toshihiko Oka, Katsuyoshi Mihara

    Journal of Cell Biology   179 ( 7 )   1355 - 1363   2007.12

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

    DOI： 10.1083/jcb.200702143

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Presentations

  • Brain-derived neurotrophic factor improves neurite development and mitochondrial activity of dopaminergic neurons differentiated from exfoliated deciduous tooth-derived pulp stem cells of children with ADHD. International conference

    #Nguyen, H.T.N., @Kato, H., @Sato, H., @Yamaza, H., @Masuda, K.

    Neuroscience 2019  2019.10 

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    Event date： 2020.1

    Language：English  

    Venue：Chicago   Country：United States  

  • メラトニンはIP3媒介性カルシウム調節を介して自閉スペクトラム症の神経発達を改善する

    董双山, KIFUNE Takashi, KATO Hiroki, WANG Lu, KONG Jun, HIROFUJI Yuta, SATO Hiroshi, ITO Yosuke, KATO Takahiro A., SAKAI Yasunari, OHGA Shouichi, FUKUMOTO Satoshi, MASUDA Keiji

    第45回日本生物学的精神医学会年会  2023.11 

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    Event date： 2024.4

    Language：Japanese  

    Country：Japan  

  • 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： 2024.4

    Language：Japanese  

    Country：Japan  

  • ヒト脱落乳歯由来幹細胞を活用したミトコンドリア病の病態解明

    韓 旭, 加藤 大樹, 山座 治義, 増田 啓二, 廣藤 雄太, 野中 和明

    第56回日本小児歯科学会大会  2018.5 

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    Event date： 2024.4

    Language：Japanese  

    Country：Japan  

  • レット症候群患児の乳歯歯髄幹細胞から分化したドーパミンニューロンに認めたミトコンドリア機能障害

    増田啓次、加藤大樹、廣藤雄太、廣藤早紀、山座治義、佐藤浩、高山扶美子、野中和明

    第40回日本生物学的精神医学会  2018.9 

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    Event date： 2024.4

    Language：Japanese  

    Country：Japan  

  • Folic acid-mediated mitochondrial activation for protection against oxidative stress in human dental pulp stem cells derived from deciduous teeth

    張虞、加藤大樹、増田啓次、山座治義、廣藤雄太、韓旭、野中和明

    第57回日本小児歯科学会大会  2019.5 

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    Event date： 2024.4

    Language：Japanese  

    Country：Japan  

  • ヒト歯髄幹細胞を用いた変容性骨異形成症の病態再現と機能解明

    韓旭、 加藤大樹、 山座治義、 廣藤雄太、 増田啓次、 福本敏

    第58回日本小児歯科学会大会  2020.4 

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    Event date： 2024.4

    Language：Japanese  

    Country：Japan  

  • GαOは細胞内カルシウム依存性シグナルを制御する

    平良遼志、赤峰哲、奥園清香、山元裕之、米元耕輔、石崎義人、實藤雅文、佐方功明、扇谷昌宏、加藤隆弘、加藤大樹、増田啓次、神庭重信、酒井康成、大賀正一

    第63回日本小児神経学会学術集会  2021.5 

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    Event date： 2024.4

    Language：Japanese  

    Country：Japan  

  • ダウン症候群の乳歯歯髄幹細胞から分化したドーパミン作動性ニューロンにおける神経突起発達とドーパミン調節障害

    孫梟、加藤大樹、韓旭、張虞、佐藤浩、加藤隆弘、酒井康成、大賀正一、福本敏、増田啓次

    第63回日本小児神経学会学術集会  2021.5 

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    Event date： 2024.4

    Language：Japanese  

    Country：Japan  

  • MFF機能不全のヒト乳歯由来幹細胞から分化したドーパミン作動性ニューロンにおけるミトコンドリアのカルシウム過負荷と酸化ストレス

    Shuangshan Dong, Xiao Sun, Hiroki Kato, Jun Kong, Yosuke Ito, Hiroshi Sato, Takahiro A. Kato, Yasunari Sakai, Satoshi Fukumoto, Keiji Masuda

    BPCNPNPPP4学会合同年会  2022.11 

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    Event date： 2024.4

    Language：Japanese  

    Country：Japan  

  • 脱落乳歯を活用したミトコンドリア病研究

    加藤大樹、韓旭、佐藤浩、山座治義、増田啓次、廣藤雄太、野中和明

    第18回日本ミトコンドリア学会年会  2018.12 

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    Event date： 2024.4

    Language：Japanese  

    Country：Japan  

  • Pathological analysis of autism spectrum disorder using deciduous tooth-derived stem cells.

    加藤大樹、Nguyen, H.T.N.、 増田啓次、山座治義、廣藤雄太、佐藤浩、Pham, T.M.T.、 高山扶美子、酒井康成、大賀正一、田口智章、野中和明

    第61回日本小児神経学会学術集会  2019.5 

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    Event date： 2024.4

    Language：English  

    Country：Japan  

  • 注意欠如多動症の男児由来の乳歯歯髄幹細胞から分化したドーパミン作動性ニューロンの神経突起成長とミトコンドリア機能の障害はBDNFにより改善する

    Nguyen, H.T.N.、加藤大樹、佐藤浩、野中和明、増田啓次

    第41回日本生物学的精神医学会  2019.6 

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    Event date： 2024.4

    Language：Japanese  

    Country：Japan  

  • HeLa細胞における21番染色体トリソミーのダイソミー化

    佐藤　浩、加藤　大樹、山座　治義、増田　啓次、Huong Thi Nguyen Nguyen, Thanh Thi Mai Pham,　韓 旭、廣藤　雄太、野中　和明

    ConBio 2017 生命科学合同年次大会  2017.12 

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    Event date： 2017.12

    Language：Japanese  

    Country：Japan  

  • Understanding of neuropathology in Down syndrome: An in vitro study utilizing stem cells from exfoliated deciduous teeth. International conference

    Thanh Thi Mai Pham, Hiroki Kato, Haruyoshi Yamaza, Keiji Masuda, Yuta Hirofuji,　Hiroshi Sato, Huong Thi Nguyen Nguyen, Tomoaki Taguchi, Kazuaki Nonaka

    The 28th FUKUOKA INTERNATIONAL SYMPOSIUM ON PEDIATRIC / MATERNAL-CHILD HEALTH RESEARCH  2017.9 

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    Event date： 2017.9

    Language：English   Presentation type：Oral presentation (general)  

    Country：Japan  

  • Etiological research of congenital disorder with stem cells from human exfoliated deciduous teeth International conference

    Hiroshi Sato, Pham Thi Mai Thanh, Xu Han, Hiroki Kato, Haruyoshi Yamaza, Keiji Masuda, Kazuaki Nonaka

    The 27th FUKUOKA INTERNATIONAL SYMPOSIUM ON PEDIATRIC / MATERNAL-CHILD HEALTH RESEARCH  2017.8 

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    Event date： 2017.8

    Language：Japanese  

    Country：Japan  

  • Increase of mitochondrial activity is crucial for the neuronal differentiation of stem cells from exfoliated deciduous teeth

    Hiroki Kato, Thanh Thi Mai Pham, Xu Han, Yuta Hirofuji, Haruyoshi Yamaza, Keiji Masuda, Hiroshi Sato, Tomoaki Taguchi, Kazuaki Nonaka

    細胞生物学会  2017.6 

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    Event date： 2017.6

    Language：Japanese  

    Venue：仙台   Country：Japan  

  • Biological relationship between mitochondrial function and osteogenesis International conference

    H. YAMAZA, H. KATO, H. XU, H. SATO, P. THANH, Y. HIROFUJI, K. MASUDA, K NONAKA

    Gordon Research Conference, Musculoskeletal Biology & Bioengineering  2016.8 

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    Event date： 2016.8

    Language：English  

    Venue：Proctor Academy   Country：United States  

  • Demand of mitochondrial activity in neuronal differentiation of stem cells from exfoliated deciduous teeth International conference

    Hiroki Kato, Pham Thi Mai Thanh, Haruyoshi Yamaza, Keiji Masuda, Hiroshi Sato, Kazuaki Nonaka

    Gordon Research Conference on Craniofacial Morphogenesis & Tissue Regeneration  2016.6 

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    Event date： 2016.3

    Language：English  

    Venue：Ventura   Country：United States  

  • Application of pulpal stem cell from exfoliated deciduous teeth to study the etiology of Rett Syndrome International conference

    Hiroki KATO, Keiko WATANABE, Haruyoshi YAMAZA, Keiji MASUDA, Hiroshi SATO and Kazuaki NONAKA

    "The Neurobiology of Parenting", Berzelius symposium 90  2015.8 

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    Event date： 2015.8

    Language：English  

    Venue：Stockholm   Country：Sweden  

  • Translational research in developmental disorder by utilizing exfoliated deciduous teeth. International conference

    Hiroki Kato, Keiko Watanabe, Haruyoshi Yamaza, Keiji Masuda, Hiroshi Sato, Kazuaki Nonaka

    The 26th FUKUOKA INTERNATIONAL SYMPOSIUM ON PEDIATRIC / MATERNAL-CHILD HEALTH RESEARCH  2015.8 

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    Event date： 2015.8 - 2018.7

    Language：English  

    Country：Japan  

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MISC

  • Dental Pulp-Derived Mesenchymal Stem Cells for Modeling Genetic Disorders. Reviewed

    Masuda, K., Han, X., Kato, H., Sato, H., Zhang, Y., Sun, X., Hirofuji, Y., Yamaza, Yamada, A., Fukumoto, S.

    Int J Mol Sci.   2021.2

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

  • プリオン病 Up to date 正常プリオン蛋白の構造と機能

    加藤 大樹、八谷　如美

    Clinical neuroscience   2013.9

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

Professional Memberships

  • The Japanese Biochemical Society

  • 日本小児歯科学会

  • 日本小児神経学会

  • 日本細胞生物学会

  • 歯科基礎医学会

  • 日本ミトコンドリア学会

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Committee Memberships

  • Asian Pacific Society of Prion Research   Councilor   Foreign country

    2011.7 - 2015.7   

Academic Activities

  • Screening of academic papers

    Role(s)： Peer review

    2022

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    Type：Peer review 

    Number of peer-reviewed articles in foreign language journals：1

  • Screening of academic papers

    Role(s)： Peer review

    2021

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    Type：Peer review 

    Number of peer-reviewed articles in foreign language journals：2

  • Screening of academic papers

    Role(s)： Peer review

    2020

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    Type：Peer review 

    Number of peer-reviewed articles in foreign language journals：2

  • Screening of academic papers

    Role(s)： Peer review

    2019

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    Type：Peer review 

    Number of peer-reviewed articles in foreign language journals：3

  • Screening of academic papers

    Role(s)： Peer review

    2018

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    Type：Peer review 

    Number of peer-reviewed articles in foreign language journals：1

  • Screening of academic papers

    Role(s)： Peer review

    2017

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    Type：Peer review 

    Number of peer-reviewed articles in foreign language journals：2

  • 事務局運営 International contribution

    THE 27th FUKUOKA INTERNATIONAL SYMPOSIUM ON PEDIATRIC/MATERNAL-CHILD HEALTH RESEARCH  （ Fukuoka Japan ） 2016.8 - 2018.8

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    Type：Competition, symposium, etc. 

  • 事務局運営

    福岡国際母子総合研究シンポジウム 第14回市民公開講座  （ Japan ） 2016.8

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    Type：Competition, symposium, etc. 

  • Screening of academic papers

    Role(s)： Peer review

    2016

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    Type：Peer review 

    Number of peer-reviewed articles in foreign language journals：1

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Research Projects

  • 疾患特異的ヒト乳歯幹細胞によるドラベ症候群の分子病態解明

    2023

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    Grant type：Donation

  • 乳歯幹細胞による稀少難病ドラベ症候群の病態解明

    Grant number：22K10275  2022 - 2024

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

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    Authorship：Principal investigator  Grant type：Scientific research funding

  • 医学系研究助成

    2022

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    Grant type：Donation

  • 学術奨励賞

    2021

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    Grant type：Donation

  • 自閉症児由来乳歯歯髄幹細胞を活用した酸化ストレスとミトコンドリアとの関係解明

    Grant number：19K10387  2019 - 2021

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

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

  • 性染色体数異常における発達障害機序の解析　～乳歯歯髄幹細胞による橋渡し研究～

    Grant number：19K10386  2019 - 2021

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

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

  • 細胞増殖から分化への転換に連関するミトコンドリア活性制御機構の解明

    Grant number：19K10406  2019 - 2021

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

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    Authorship：Principal investigator  Grant type：Scientific research funding

  • 乳歯で染色体異常疾患を克服するトランスレーショナル研究

    Grant number：16K15839  2016 - 2018

    Grants-in-Aid for Scientific Research  Grant-in-Aid for challenging Exploratory Research

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

  • 酸化ストレスからみた口唇裂口蓋裂発症機序解明と予防法の開発

    Grant number：16K11807  2016 - 2018

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

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    Authorship：Principal investigator  Grant type：Scientific research funding

  • 医学系研究助成

    2015

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    Grant type：Donation

  • 研究助成金

    2015

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    Grant type：Donation

  • ミトコンドリア凝集が引き起こす神経細胞死メカニズムの解明

    Grant number：25860224  2013 - 2014

    Grants-in-Aid for Scientific Research  Grant-in-Aid for Young Scientists (B)

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    Authorship：Principal investigator  Grant type：Scientific research funding

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Educational Activities

  • 学部および大学院の学生教育

Class subject

  • 解剖学

    2024.4 - 2025.3   Full year

  • 解剖学

    2023.4 - 2024.3   Full year

  • 解剖学

    2022.4 - 2023.3   Full year

  • リサーチエクスポージャ

    2022.4 - 2022.6   Spring quarter

  • リサーチエクスポージャ4

    2021.12 - 2022.2   Winter quarter

  • リサーチエクスポージャ3

    2021.10 - 2021.12   Fall quarter

  • リサーチエクスポージャ2

    2021.6 - 2021.8   Summer quarter

  • 解剖学

    2021.4 - 2022.3   Full year

  • リサーチエクスポージャ1

    2021.4 - 2021.6   Spring quarter

  • 解剖学

    2020.10 - 2021.3   Second semester

  • リサーチエクスポージャ

    2020.10 - 2021.3   Second semester

  • 発生学

    2020.4 - 2020.9   First semester

  • アーリーエクスポージャ

    2020.4 - 2020.9   First semester

  • 小児口腔医学

    2019.4 - 2020.3   Full year

  • 小児口腔医学演習

    2019.4 - 2020.3   Full year

  • 小児口腔医学

    2019.4 - 2020.3   Full year

  • 小児歯科学

    2019.4 - 2020.3   Full year

  • Special Need Dentistry

    2019.4 - 2019.9   First semester

  • Pediatric Dentistry

    2019.4 - 2019.9   First semester

  • 小児歯科学

    2018.4 - 2019.3   Full year

  • 小児口腔医学

    2018.4 - 2019.3   Full year

  • 小児口腔医学演習

    2018.4 - 2019.3   Full year

  • Pediatric Dentistry

    2018.4 - 2018.9   First semester

  • Special Need Dentistry

    2018.4 - 2018.9   First semester

  • 小児歯科学

    2017.4 - 2018.3   Full year

  • 小児口腔医学

    2017.4 - 2018.3   Full year

  • 小児口腔医学演習

    2017.4 - 2018.3   Full year

  • Pediatric Dentistry

    2017.4 - 2017.9   First semester

  • Special Need Dentistry

    2017.4 - 2017.9   First semester

  • 小児歯科学

    2016.4 - 2017.3   Full year

  • 小児口腔医学

    2016.4 - 2017.3   Full year

  • 小児口腔医学演習

    2016.4 - 2017.3   Full year

  • Pediatric Dentistry

    2016.4 - 2016.9   First semester

  • Special Need Dentistry

    2016.4 - 2016.9   First semester

  • 小児歯科学

    2015.4 - 2016.3   Full year

  • 小児口腔医学

    2015.4 - 2016.3   Full year

▼display all

FD Participation

  • 2024.6   Role：Participation   Title：歯科医師国家試験合格率アップのための戦略

    Organizer：[Undergraduate school/graduate school/graduate faculty]

  • 2020.6   Role：Participation   Title：ジャーナルをめぐる現状と論文の投稿・入手について

    Organizer：[Undergraduate school/graduate school/graduate faculty]

  • 2019.9   Role：Participation   Title：科研費申請のススメ！〜科学研究費補助金制度と研究計画調書作成時の注意点〜

    Organizer：[Undergraduate school/graduate school/graduate faculty]

  • 2018.5   Role：Participation   Title：平成３０年度第1回歯学研究院FD 「臨床実習後臨床能力試験トライアルの実施に向けて」

    Organizer：[Undergraduate school/graduate school/graduate faculty]

  • 2018.3   Role：Participation   Title：平成２９年度第２回歯学研究院FD「東京医歯大における国家試験対策の実践」

    Organizer：[Undergraduate school/graduate school/graduate faculty]

Travel Abroad

  • 2008.10 - 2011.3

    Staying countory name 1：Germany   Staying institution name 1：Universität Tübingen