Updated on 2024/12/24

写真a

 
NISHIDA Takashi
 
Organization
Faculty of Medicine, Dentistry and Pharmaceutical Sciences Associate Professor
Position
Associate Professor
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Degree

  • 博士(歯学) ( 岡山大学 )

Research Interests

  • メカノバイオロジー

  • 骨代謝研究

  • Cartilage biology

Research Areas

  • Life Science / Oral biological science

Education

  • 岡山大学大学院   歯学研究科  

    1995.4 - 1999.3

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    Country: Japan

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  • Okayama University   歯学部   歯学

    1989.4 - 1995.3

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    Country: Japan

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Research History

  • Associate Professor,Graduate School of Medicine, Dentistry and Pharmaceutical Sciences,Okayama University

    2014.10

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  • 岡山大学大学院医歯薬学総合研究科 助教

    2005.9 - 2014.9

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  • University of California, Los Angeles

    2004.4 - 2005.9

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  • 岡山大学大学院医歯学総合研究科 助手

    2001.4 - 2004.3

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  • 岡山大学 歯学部 教務員

    1999.4 - 2001.3

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Professional Memberships

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Committee Memberships

  • 日本歯科基礎医学会   評議員  

    2015   

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    Committee type:Academic society

    日本歯科基礎医学会

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  • 岡山歯学会   評議員  

    2014   

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    Committee type:Academic society

    岡山歯学会

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  • 日本CCNファミリー研究会   会場の管理、運営  

    2007   

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    Committee type:Academic society

    日本CCNファミリー研究会

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  • 日本軟骨代謝学会   評議員  

       

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    Committee type:Academic society

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Papers

  • Expression and function of CCN2-derived circRNAs in chondrocytes Reviewed

    Soma Kato, Kazumi Kawata, Takashi Nishida, Tomomi Mizukawa, Masaharu Takigawa, Seiji Iida, Satoshi Kubota

    Journal of Cell Communication and Signaling   2023.9

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    Publishing type:Research paper (scientific journal)   Publisher:Springer Science and Business Media LLC  

    Abstract

    Cellular communication network factor 2 (CCN2) molecules promote endochondral ossification and articular cartilage regeneration, and circular RNAs (circRNAs), which arise from various genes and regulate gene expression by adsorbing miRNAs, are known to be synthesized from CCN2 in human vascular endothelial cells and other types of cells. However, in chondrocytes, not only the function but also the presence of CCN2-derived circRNA remains completely unknown. In the present study, we investigated the expression and function of CCN2-derived circRNAs in chondrocytes. Amplicons smaller than those from known CCN2-derived circRNAs were observed using RT-PCR analysis that could specifically amplify CCN2-derived circRNAs in human chondrocytic HCS-2/8 cells. The nucleotide sequences of the PCR products indicated novel circRNAs in the HCS-2/8 cells that were different from known CCN2-derived circRNAs. Moreover, the expression of several Ccn2-derived circRNAs in murine chondroblastic ATDC5 cells was confirmed and observed to change alongside chondrocytic differentiation. Next, one of these circRNAs was knocked down in HCS-2/8 cells to investigate the function of the human CCN2-derived circRNA. As a result, CCN2-derived circRNA knockdown significantly reduced the expression of aggrecan mRNA and proteoglycan synthesis. Our data suggest that CCN2-derived circRNAs are expressed in chondrocytes and play a role in chondrogenic differentiation.

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    DOI: 10.1007/s12079-023-00782-7

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    Other Link: https://link.springer.com/article/10.1007/s12079-023-00782-7/fulltext.html

  • Dual roles of cellular communication network factor 6 (CCN6) in the invasion and metastasis of oral cancer cells to bone via binding to BMP2 and RANKL Reviewed

    Hiroaki Hochi, Satoshi Kubota, Masaharu Takigawa, Takashi Nishida

    Carcinogenesis   2023.8

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    Authorship:Corresponding author   Publishing type:Research paper (scientific journal)   Publisher:Oxford University Press (OUP)  

    Abstract

    The acquisition of motility via epithelial–mesenchymal transition (EMT) and osteoclast induction are essential for the invasion and metastasis of oral squamous cell carcinoma (OSCC) to bone. However, the molecule suppressing both EMT and osteoclastogenesis is still unknown. In this study, we found that cellular communication network factor 6 (CCN6) was less produced in a human OSCC cell line, HSC-3 with mesenchymal phenotype, than in HSC-2 cells without it. Notably, CCN6 interacted with bone morphogenetic protein 2 (BMP2) and suppressed the cell migration of HSC-3 cells stimulated by BMP2. Moreover, knockdown of CCN6 in HSC-2 cells led to the promotion of EMT and enhanced the effect of transforming growth factor-β (TGF-β) on the promotion of EMT. Furthermore, CCN6 combined with BMP2 suppressed EMT. These results suggest that CCN6 strongly suppresses EMT in cooperation with BMP2 and TGF-β. Interestingly, CCN6 combined with BMP2 increased the gene expression of receptor activator of nuclear factor-κB ligand (RANKL) in HSC-2 and HSC-3 cells. Additionally, CCN6 interacted with RANKL, and CCN6 combined with RANKL suppressed RANKL-induced osteoclast formation. In metastatic lesions, increasing BMP2 due to the bone destruction led to interference with binding of CCN6 to RANKL, which results in the promotion of bone metastasis of OSCC cells due to continuous osteoclastogenesis. These findings suggest that CCN6 plays dual roles in the suppression of EMT and in the promotion of bone destruction of OSCC in primary and metastatic lesions, respectively, through cooperation with BMP2 and interference with RANKL.

    DOI: 10.1093/carcin/bgad057

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  • Do not overwork: cellular communication network factor 3 for life in cartilage. Reviewed International journal

    Satoshi Kubota, Harumi Kawaki, Bernard Perbal, Masaharu Takigawa, Kazumi Kawata, Takako Hattori, Takashi Nishida

    Journal of cell communication and signaling   17 ( 2 )   353 - 359   2023.6

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

    Cellular communication network factor (CCN) 3, which is one of the founding members of the CCN family, displays diverse functions. However, this protein generally represses the proliferation of a variety of cells. Along with skeletal development, CCN3 is produced in cartilaginous anlagen, growth plate cartilage and epiphysial cartilage. Interestingly, CCN3 is drastically induced in the growth plates of mice lacking CCN2, which promotes endochondral ossification. Notably, chondrocytes in these mutant mice with elevated CCN3 production also suffer from impaired glycolysis and energy metabolism, suggesting a critical role of CCN3 in cartilage metabolism. Recently, CCN3 was found to be strongly induced by impaired glycolysis, and in our study, we located an enhancer that mediated CCN3 regulation via starvation. Subsequent investigations specified regulatory factor binding to the X-box 1 (RFX1) as a transcription factor mediating this CCN3 regulation. Impaired glycolysis is a serious problem, resulting in an energy shortage in cartilage without vasculature. CCN3 produced under such starved conditions restricts energy consumption by repressing cell proliferation, leading chondrocytes to quiescence and survival. This CCN3 regulatory system is indicated to play an important role in articular cartilage maintenance, as well as in skeletal development. Furthermore, CCN3 continues to regulate cartilage metabolism even during the aging process, probably utilizing this regulatory system. Altogether, CCN3 seems to prevent "overwork" by chondrocytes to ensure their sustainable life in cartilage by sensing energy metabolism. Similar roles are suspected to exist in relation to systemic metabolism, since CCN3 is found in the bloodstream.

    DOI: 10.1007/s12079-023-00723-4

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  • Novel Cell Biological Assays for Measuring Bone 2 Remodeling Activities of CCN Proteins Reviewed International journal

    Takashi Nishida, Satoshi Kubota, Masaharu Takigawa

    Methods in molecular biology (Clifton, N.J.)   2582   255 - 268   2023

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    Authorship:Lead author   Language:English   Publishing type:Part of collection (book)  

    Although two-dimensional (2D) cultures from bone lineage cells are often used, it is well-known that this culture system is completely different from the in vivo bone matrix environment. In this paper, we describe a 3D culture method using both the mouse osteocytic cell line, MLO-Y4, and an osteocyte-enriched population of the cells isolated from mice. These cells are embedded in collagen gel with recombinant cellular communication network (CCN) factor proteins; then, osteoblasts or osteoclasts are inoculated and cultured on the collagen gel. Because this method mimics the in vitro bone matrix environment, it is useful for understanding the detailed mechanism of actions of CCN proteins in the bone matrix.

    DOI: 10.1007/978-1-0716-2744-0_17

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  • Fibroblast Growth Factors and Cellular Communication Network Factors: Intimate Interplay by the Founding Members in Cartilage Reviewed

    Kubota S, Aoyama E, Takigawa M, Nishida T

    Int J Mol Sci.   23 ( 15 )   8592   2022.8

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Books

  • Novel Cell Biological Assays for Measuring Bone Remodeling Activities of CCN Proteins

    Nishida, T, Takigawa, M, Kubota, S( Role: Joint author)

    Springer  2022.12 

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  • Effect of CCN2 on the osteocyte function regulating the osteoclast formation and its possibility as a novel drug of osteoporosis

    ( Role: Joint author)

    2016 

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    Language:Japanese

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  • Cell biological assays for measuring chondrogenic activities of CCN2 protein

    Nishida, T., Kubota, S. and Takigawa, M.( Role: Joint author)

    Springer  2016 

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    Responsible for pages:1489, 219-237   Language:English

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  • Production of recombinant CCN2 protein by mammalian cells

    Nishida T, Kubota S, Takigawa M.( Role: Joint author)

    Springer  2016 

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    Responsible for pages:1489, 95-105,   Language:English

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  • CCN2による骨細胞機能を標的とした新規骨粗鬆症治療薬の開発

    科学研究費助成事業  2016 

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MISC

  • Promotion of the osteogenic differentiation of mesenchymal stem cells via CCN1 increasing by low-Intensity pulsed ultrasound (LIPUS) combined with BMP-2.

    Hsu Myat Paing, Takashi Nishida, Masaharu Takigawa, Takuo Kuboki, Satoshi Kubota

    2024.12

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  • 霊長類特異的long non coding RNA, urothelial cancer associated 1のCRISPR-CAS9を用いたknock-inマウスの作製とゲノム中でのUCA1の不安定性。

    近藤 星, 桑原実穂, Fu, S., Selvam Kavitha Panneer, Janvier Habumugisha, 大野充昭, 藤井匡寛, 西田 崇, 久保田聡, 服部高子

    第47回日本分子生物学会抄録集   2024.11

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  • 霊長類特異的long non coding urothelial cancer associated 1 (UCA1)のCRISPR-CAS9を用いたknock-inマウスの作製とその解析。

    近藤 星, 桑原実穂, Shanqi, Fu, Kavitha, Panneer Selvam, Janvier Habumugisha, 大野充昭, 藤井匡寛, 西田 崇, 久保田聡, 服部高子

    第97回日本生化学会抄録集   2024.11

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  • Low-Intensity Pulsed Ultrasound (LIPUS) enhances the osteogenic differentiation of mesenchymal stem cells in cooperation with Bone Morphogenetic Protein-2 (BMP-2).

    Paing, H.M., Nishida, T., Takigawa, M., Takuo Kuboki, T., Kubota, S.

    2024.8

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  • 核内CCN2は転写共役因子として関節軟骨の維持に作用する。

    西田 崇, 長尾由里香, 滝川正春, 久保田聡

    第15回日本CCNファミリー研究会抄録集   2024.8

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Presentations

  • Expression and function of CCN2-derived circRNAs in chondrocytes.

    2023.12.7 

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    Event date: 2023.12.6 - 2023.12.8

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

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  • 軟骨細胞におけるCCN2由来circRNAの発現とその機能の可能性

    加藤壮真, 河田かずみ, 西田 崇, 滝川正春, 久保田聡

    第65回歯科基礎医学会  2023.9.18 

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    Event date: 2023.9.16 - 2023.9.18

    Language:Japanese  

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  • 軟骨細胞におけるCCN2の核移行の意義

    西田 崇, 滝川正春, 久保田聡

    第14回日本CCNファミリー研究会  2023.9.2 

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    Event date: 2023.9.2

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  • CCN6はBMP2による口腔がん細胞の上皮・間葉転換をコントロールする

    芳地浩彰, 久保田聡, 滝川正春, 西田 崇

    第14回日本CCNファミリー研究会  2023.9.2 

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    Event date: 2023.9.2

    Language:Japanese   Presentation type:Oral presentation (general)  

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  • 線維化におけるCCN2の転写共役因子としての作用

    西田 崇, 辰川ひなた, 滝川正春, 久保田聡

    第55回日本結合組織学会  2023.6.25 

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    Event date: 2023.6.24 - 2023.6.25

    Language:Japanese   Presentation type:Oral presentation (general)  

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Awards

  • 研究奨励賞

    2011.7   日本骨代謝学会  

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    Country:Japan

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Research Projects

  • Investigation on phase separation-mediated regulation of cell differentiation by droplet transpricptomics

    Grant number:24H00652  2024.04 - 2027.03

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

    久保田 聡, 西田 崇, 服部 高子, 高江洲 かずみ, 滝川 正春, 青山 絵理子, 大野 充昭

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    Grant amount:\48100000 ( Direct expense: \37000000 、 Indirect expense:\11100000 )

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  • 糖代謝障害が招く軟骨肥大性細胞老化を介したO Aの発症機構の解明とC C N2の役割

    Grant number:24K12869  2024.04 - 2027.03

    日本学術振興会  科学研究費助成事業  基盤研究(C)

    西田 崇, 服部 高子, 青山 絵理子, 高江洲 かずみ, 滝川 正春, 久保田 聡

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    Grant amount:\4550000 ( Direct expense: \3500000 、 Indirect expense:\1050000 )

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  • Development of dropletomics that clarifies transcriptional regulation under liquid-liquid phase separation

    Grant number:23K17439  2023.06 - 2027.03

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

    久保田 聡, 西田 崇, 服部 高子, 高江洲 かずみ, 滝川 正春, 青山 絵理子, 大野 充昭

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    Grant amount:\25740000 ( Direct expense: \19800000 、 Indirect expense:\5940000 )

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  • 象牙芽細胞の表面に突き出た細胞小器官の機能解析と象牙質再生への応用

    Grant number:22K10075  2022.04 - 2025.03

    日本学術振興会  科学研究費助成事業  基盤研究(C)

    高江洲 かずみ, 服部 高子, 青山 絵理子, 滝川 正春, 西田 崇, 久保田 聡

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    Grant amount:\4290000 ( Direct expense: \3300000 、 Indirect expense:\990000 )

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  • 非コードRNAを介した新たな軟骨ホメオスタシスとその変性メカニズムの解明

    Grant number:22K10218  2022.04 - 2025.03

    日本学術振興会  科学研究費助成事業  基盤研究(C)

    森谷 徳文, 滝川 正春, 久保田 聡, 服部 高子, 西田 崇, 近藤 星

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    Grant amount:\4160000 ( Direct expense: \3200000 、 Indirect expense:\960000 )

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Class subject in charge

  • From molecules to organisms (2024academic year) Third semester  - 金5~6

  • Molecular Dentistry (2024academic year) 3rd and 4th semester  - [第3学期]水4, [第4学期]月4

  • Molecular Biology and Biochemistry of Signal Transduction (2024academic year) Second semester  - 木1,木2,木3

  • Molecular Dentistry Demonstration (2024academic year) Fourth semester  - 水4,水5,水6,水7,木1,木2,木3

  • Seminar in Biochemistry and Molecular Dentistry (2024academic year) Fourth semester  - 水4,水5,水6,水7,木1,木2,木3

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