YODA Masaki

写真a

Affiliation

School of Medicine, Department of Orthopaedic Surgery (Shinanomachi)

Position

Project Assistant Professor (Non-tenured)/Project Research Associate (Non-tenured)/Project Instructor (Non-tenured)

External Links

Career 【 Display / hide

  • 2019.04
    -
    Present

    慶應義塾大学, 医学部 整形外科学, 特任助教

  • 2016.04
    -
    2019.03

    慶應義塾大学, 医学部 共同利用研究室 細胞組織学研究室, 助教

  • 2007.01
    -
    2016.03

    慶應義塾大学, 医学部 抗加齢運動器楽寄付講座(整形外科学), 特任助教

Academic Background 【 Display / hide

  • 1997.04
    -
    2003.03

    Tohoku University, 農学研究科, 資源生物科学専攻

    日本, Graduate School, Completed, Doctoral course

Academic Degrees 【 Display / hide

  • 博士(農学), Tohoku University, Coursework, 2003.03

    サケ科魚類におけるテロメラーゼ活性の発現に関する研究

 

Research Areas 【 Display / hide

  • General physiology

  • Orthopaedic surgery

Research Keywords 【 Display / hide

  • 筋代謝

  • 骨代謝

  • 軟骨代謝

  • 運動器学

 

Papers 【 Display / hide

  • Innervation of the tibial epiphysis through the intercondylar foramen

    Matsuo K., Ji S., Miya A., Yoda M., Hamada Y., Tanaka T., Takao-Kawabata R., Kawaai K., Kuroda Y., Shibata S.

    Bone (Elsevier)  120   297 - 304 2019.03

    Research paper (scientific journal), Joint Work, Accepted,  ISSN  87563282

     View Summary

    The periosteum and mineralized bone are innervated by nerves that sense pain. These include both myelinated and unmyelinated neurons with either free nerve endings or bearing nociceptors. Parasympathetic and sympathetic autonomic nerves also innervate bone. However, little is known about the route sensory nerves take leaving the epiphyses of long bones at the adult knee joint. Here, we used transgenic mice that express fluorescent Venus protein in Schwann cells (Sox10-Venus mice) to visualize myelinated and unmyelinated nerves in the tibial epiphysis. Immunofluorescence to detect a pan-neuronal marker and the sensory neuron markers calcitonin gene-related peptide (CGRP) and tropomyosin receptor kinase A (TrkA) also revealed Schwann cell-associated sensory neurons. Foramina in the intercondylar area of the tibia were conserved between rodents and primates. Venus-labeled fibers were detected within bone marrow of the proximal epiphysis, exited through foramina along with blood vessels in the intercondylar area of the tibia, and joined Venus-labeled fibers of the synovial membrane and meniscus. These data suggest that innervation of the subchondral plate and trabecular bone within the tibial epiphysis carries pain signals from the knee joint to the brain through intercondylar foramina.

  • Trans-pairing between osteoclasts and osteoblasts shapes the cranial base during development

    Edamoto M., Kuroda Y., Yoda M., Kawaai K., Matsuo K.

    Scientific Reports (Springer Nature)  9 ( 1 )  2019.02

    Research paper (scientific journal), Joint Work, Accepted

     View Summary

    Bone growth is linked to expansion of nearby organs, as is the case for the cranial base and the brain. Here, we focused on development of the mouse clivus, a sloping surface of the basioccipital bone, to define mechanisms underlying morphological changes in bone in response to brain enlargement. Histological analysis indicated that both endocranial and ectocranial cortical bone layers in the basioccipital carry the osteoclast surface dorsally and the osteoblast surface ventrally. Finite element analysis of mechanical stress on the clivus revealed that compressive and tensile stresses appeared mainly on respective dorsal and ventral surfaces of the basioccipital bone. Osteoclastic bone resorption occurred primarily in the compression area, whereas areas of bone formation largely coincided with the tension area. These data collectively suggest that compressive and tensile stresses govern respective localization of osteoclasts and osteoblasts. Developmental analysis of the basioccipital bone revealed the clivus to be angled in early postnatal wild-type mice, whereas its slope was less prominent in Tnfsf11 −/− mice, which lack osteoclasts. We propose that osteoclast-osteoblast “trans-pairing” across cortical bone is primarily induced by mechanical stress from growing organs and regulates shape and size of bones that encase the brain.

  • Granulocyte-colony stimulating factor enhances load-induced muscle hypertrophy in mice

    Ohashi M., Okubo K., Mizuno S., Yoda M., Shirasawa H., Chiba K., Horiuchi K., Matsumoto M., Nakamura M.

    Biochemical and Biophysical Research Communications (Elsevier)  506 ( 4 ) 944 - 949 2018.12

    Research paper (scientific journal), Joint Work, Accepted,  ISSN  0006291X

     View Summary

    Granulocyte-colony stimulating factor (G-CSF) is a cytokine crucially involved in the regulation of granulopoiesis and the mobilization of hematopoietic stem cells from bone marrow. However, emerging data suggest that G-CSF exhibits more diverse functions than initially expected, such as conferring protection against apoptosis to neural cells and stimulating mitogenesis in cardiomyocytes and skeletal muscle stem cells after injury. In the present study, we sought to investigate the potential contribution of G-CSF to the regulation of muscle volume. We found that the administration of G-CSF significantly enhances muscle hypertrophy in two different muscle overload models. Interestingly, there was a significant increase in the transcripts of both G-CSF and G-CSF receptors in the muscles that were under overload stress. Using mutant mice lacking the G-CSF receptor, we confirmed that the anabolic effect is dependent on the G-CSF receptor signaling. Furthermore, we found that G-CSF increases the diameter of myotubes in vitro and induces the phosphorylation of AKT, mTOR, and ERK1/2 in the myoblast-like cell line C2C12 after differentiation induction. These findings indicate that G-CSF is involved in load-induced muscle hypertrophy and suggest that G-CSF is a potential agent for treating patients with muscle loss and sarcopenia.

  • Targeted ablation of p38α MAPK suppresses denervation-induced muscle atrophy

    Yuasa Kazuki, Okubo Kazumasa, Yoda Masaki, Otsu Kinya, Ishii Yasuyuki, Nakamura Masaya, Itoh Yoshiki, Horiuchi Keisuke

    Scientific Reports (Springer Nature)  8 ( 1 )  2018.12

    Research paper (scientific journal), Joint Work, Accepted,  ISSN  2045-2322

     View Summary

    The loss of skeletal muscle mass is a major cause of falls and fractures in the elderly, leading to compromised independence and a decrease in the quality of life. However, only a few therapeutic interventions leading to marginal clinical benefits in patients with this condition are currently available. Therefore, the demand to further understand the pathology of muscle atrophy and establish a treatment modality for patients with muscle atrophy is significant. p38α mitogen-activated protein kinase (p38α MAPK) is a ubiquitous signaling molecule that is implicated in various cellular functions, including cell proliferation, differentiation, and senescence. In the present study, we generated a mutant line in which p38α MAPK is specifically abrogated in muscle tissues. Compared with the control mice, these mutant mice are significantly resistant to denervation-induced muscle atrophy, suggesting that p38α MAPK positively regulates muscle atrophy. We also identified CAMK2B as a potential downstream target of p38α MAPK and found that the pharmacological inhibition of CAMK2B activity suppresses denervation-induced muscle atrophy. Altogether, our findings identify p38α MAPK as a novel regulator of muscle atrophy and suggest that the suppression of intracellular signaling mediated by p38α MAPK serves as a potential target for the treatment of muscle atrophy.

  • Inhibition of ADAM10 in satellite cells accelerates muscle regeneration following muscle injury

    Mizuno S, Yoda M, Shimoda M, Chiba K, Nakamura M, Horiuchi K

    Journal of Orthopaedic Research (Wiley)  36 ( 8 ) 2259 - 2265 2018

    Research paper (scientific journal), Joint Work, Accepted,  ISSN  07360266

     View Summary

    Muscle injury is one of the most common orthopedic and sports disorders. For severe cases, surgical repair may be indicated; however, other than immobilization and the administration of anti-inflammatory drugs there is currently no effective conservative treatment for this condition. Satellite cells (SCs) are muscle-specific stem cells and are indispensable for muscle regeneration after muscle injury. SCs are activated upon muscle injury to proliferate and differentiate into myoblasts, which subsequently fuse into myofibers and regenerate the damaged muscle. We have previously shown that ADAM10, a membrane-anchored proteolytic enzyme, is essential for the maintenance of SC quiescence by activating the Notch signaling pathway in SCs. Because suppression of ADAM10 activity in SCs can activate SC differentiation, we asked whether inactivation of ADAM10 in SCs after muscle injury could enhance muscle regeneration. Using Adam10 conditional knockout mice, in which ADAM10 activity can specifically be suppressed in SCs, we found that partial inactivation of ADAM10 accelerates muscle regeneration after muscle injury. Nearly identical results were obtained by the administration of GI254023X, a selective ADAM10 inhibitor. The findings of the present study thus indicate that transient enhancement of SC differentiation after muscle injury expedites muscle regeneration and that ADAM10 can be a potential molecular target in treating muscle injuries.

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Papers, etc., Registered in KOARA 【 Display / hide

Presentations 【 Display / hide

  • Bone formation site of mouse fibula transitions with growth

    Yoda Masaki, Kuroda Yukiko, Matsuo Koichi

    第36回日本骨代謝学会学術集会 (長崎、日本) , 2018.07, Poster (general)

  • Bone Renovation of the Mouse Neonatal Fibula into the Adult Skeleton

    Yoda Masaki, Kuroda Yukiko, Matsuo, Koichi

    America Society for Bone and Mineral Research 2017 Annual Meeting (Denver, CO, USA) , 2017.09, Poster (general)

  • Reshaping of the mouse fibula after endochondral ossification

    Yoda Masaki, Kuroda Yukiko, Matsuo Koichi

    The 35th Annual Meeting of the Japanese Society for Bone and Mineral Research (Fukuoka, Japan) , 2017.07, Oral Presentation(general)

  • 軟骨細胞におけるADAM10-Notchシグナルの抑制は顕著な成長障害を来たす

    Abrogation of ADAM10 in chondrocytes results in severe dwarfism

    The 28th Annual Meeting of the Japanese Society of Cartilage Metabolism (Tokyo, Japan) , 2015.03, Oral Presentation(general)

  • 軟骨細胞特異的なADAM10-Notchシグナルの抑制は顕著な成長障害を来たす

    依田昌樹、水野早季子、秋山治彦、松本守雄、戸山芳昭、堀内圭輔

    第32回日本骨代謝学会学術集会 (Osaka, Japan) , 2014.07, Poster (general)

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Research Projects of Competitive Funds, etc. 【 Display / hide

  • 3次元濃度勾配を有する細胞培養実現のための徐放性磁気ビーズの開発

    2017.10
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    2018.09

    JSR Corporation, Academic Development Project, 依田 昌樹, Principal Investigator

  • 軟骨原基を形成する形態形成関連因子の三次元的解析

    2017.04
    -
    2020.03

    MEXT,JSPS, Grant-in-Aid for Scientific Research, 依田 昌樹, Grant-in-Aid for Scientific Research (C), Principal Investigator

  • Regulation of bone and cartilage formation by ADAM10

    2014.04
    -
    2017.03

    MEXT,JSPS, Grant-in-Aid for Scientific Research, 依田 昌樹, Grant-in-Aid for Scientific Research (C), Principal Investigator

     View Summary

    In this study, we analyzed the regulation mechanisms of bone / cartilage formation and osteoclast differentiation by membrane type metalloprotease ADAM10. Analysis of mice abrogated ADAM10 in cartilage revealed that ADAM10 is essential for final differentiation of chondrocytes. In addition, analysis of osteoblast-specific ADAM10 deficient mice revealed that these mice indicated an increase in TSLP concentration in the serum and exhibited severe dermatitis. Furthermore, the experiment for osteoclast differentiation using osteoclast precursor lacking ADAM10 revealed that the signaling from Notch receptor, which is one of substrates for ADAM10, on the cell membrane of osteoclast precursor completely suppresses osteoclast differentiation.

  • 筋・骨格形成および造血におけるシェディングの機能解析

    2012.04
    -
    2016.03

    MEXT,JSPS, Grant-in-Aid for Scientific Research, 堀内 圭輔, Grant-in-Aid for Scientific Research (B), Co-investigator

     View Summary

    本研究では膜型タンパク質分解酵素ADAM17およびADAM10の機能を多岐にわたって解析を行った.本研究結果から,1)ADAM17が成長軟骨の吸収を制御していること,2)ADAM17はIL-1のⅡ型受容体を特異的に切断し,IL-1シグナルを正に制御しうること,また3)ADAM17その活性が転写・翻訳レベルでの制御をほとんど受けないことを明らかにした.一方,ADAM10に関しては,筋衛星細胞の恒常性維持に必須であることを解明した.またこれらの研究と並行し,破骨細胞における小胞体ストレスの機能を解析し,小胞体ストレスセンサーIRE1αを介し破骨細胞分化を制御することを明らかにした。

  • Notchシグナリングが関与する骨代謝調節機構の解明

    2012.04
    -
    2013.03

    The Nakatomi Fundation, 研究助成事業, 依田 昌樹, 研究助成金, Principal Investigator

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Awards 【 Display / hide

  • 優秀ポスター賞

    2014.07, 日本骨代謝学会, 軟骨細胞特異的なADAM10-Notchシグナルの抑制は 顕著な成長障害を来たす

    Type of Award: Awards of National Conference, Council and Symposium.  Country: Japan

  • Young Investigator Award

    2005.06, Society for Mucosal Immunology

    Type of Award: Awards of International Conference, Council and Symposium.  Country: USA