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Faculty of Medicine Center for the Support and Development of Medical Professionals Department of Clinical Education |
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FUNAMOTO Taro
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Papers 【 display / non-display 】
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Tmem161a regulates bone formation and bone strength through the P38 MAPK pathway Reviewed
Nagai T., Sekimoto T., Kurogi S., Ohta T., Miyazaki S., Yamaguchi Y., Tajima T., Chosa E., Imasaka M., Yoshinobu K., Araki K., Araki M., Choijookhuu N., Sato K., Hishikawa Y., Funamoto T.
Scientific Reports 13 ( 1 ) 14639 2023.12
Authorship：Corresponding author Language：English Publishing type：Research paper (scientific journal) Publisher：Scientific Reports
Bone remodeling is an extraordinarily complex process involving a variety of factors, such as genetic, metabolic, and environmental components. Although genetic factors play a particularly important role, many have not been identified. In this study, we investigated the role of transmembrane 161a (Tmem161a) in bone structure and function using wild-type (WT) and Tmem161a-depleted (Tmem161aGT/GT) mice. Mice femurs were examined by histological, morphological, and bone strength analyses. Osteoblast differentiation and mineral deposition were examined in Tmem161a-overexpressed, -knockdown and -knockout MC3T3-e1 cells. In WT mice, Tmem161a was expressed in osteoblasts of femurs; however, it was depleted in Tmem161aGT/GT mice. Cortical bone mineral density, thickness, and bone strength were significantly increased in Tmem161aGT/GT mice femurs. In MC3T3-e1 cells, decreased expression of alkaline phosphatase (ALP) and Osterix were found in Tmem161a overexpression, and these findings were reversed in Tmem161a-knockdown or -knockout cells. Microarray and western blot analyses revealed upregulation of the P38 MAPK pathway in Tmem161a-knockout cells, which referred as stress-activated protein kinases. ALP and flow cytometry analyses revealed that Tmem161a-knockout cells were resistant to oxidative stress. In summary, Tmem161a is an important regulator of P38 MAPK signaling, and depletion of Tmem161a induces thicker and stronger bones in mice.
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Miyazaki Shihoko, Funamoto Taro, Sekimoto Tomohisa, Kurogi Syuji, Ohta Tomomi, Nagai Takuya, Tajima Takuya, Imasaka Mai, Yoshinobu Kumiko, Araki Kimi, Araki Masatake, Choijookhuu Narantsog, Hishikawa Yoshitaka, Chosa Etsuo
ACTA HISTOCHEMICA ET CYTOCHEMICA 55 ( 3 ) 99 - 110 2022
Language：English Publishing type：Research paper (scientific journal) Publisher：JAPAN SOCIETY OF HISTOCHEMISTRY AND CYTOCHEMISTRY
Epithelial protein lost in neoplasm (EPLIN) is an actin-associated cytoskeletal protein that plays an important role in epithelial cell adhesion. EPLIN has two isoforms: EPLINα and EPLINβ. In this study, we investigated the role of EPLINβ in osteoblasts using EPLINβ-deficient (<i>EPLINβ<sup>GT/GT</sup></i>) mice. The skeletal phenotype of <i>EPLINβ<sup>GT/GT</sup></i> mice is indistinguishable from the wildtype (WT), but bone properties and strength were significantly decreased compared with WT littermates. Histomorphological analysis revealed altered organization of bone spicules and osteoblast cell arrangement, and decreased alkaline phosphatase activity in <i>EPLINβ<sup>GT/GT</sup></i> mouse bones. Transmission electron microscopy revealed wider intercellular spaces between osteoblasts in <i>EPLINβ<sup>GT/GT</sup></i> mice, suggesting aberrant cell adhesion. In <i>EPLINβ<sup>GT/GT</sup></i> osteoblasts, α- and β-catenins and F-actin were observed at the cell membrane, but OB-cadherin was localized at the perinuclear region, indicating that cadherin-catenin complexes were not formed. EPLINβ knockdown in MC3T3-e1 osteoblast cells showed similar results as in calvaria cell cultures. Bone formation markers, such as <i>RUNX2</i>, <i>Osterix</i>, <i>ALP</i>, and <i>Col1a1</i> mRNA were reduced in EPLINβ knockdown cells, suggesting an important role for EPLINβ in osteoblast formation. In conclusion, we propose that EPLINβ is involved in the assembly of cadherin-catenin complexes in osteoblasts and affects bone formation.
DOI： 10.1267/ahc.22-00027
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Kurogi S., Sekimoto T., Funamoto T., Ota T., Nakamura S., Nagai T., Nakahara M., Yoshinobu K., Araki K., Araki M., Chosa E.
Scientific Reports 7 40692 2017.1
Language：English Publishing type：Research paper (scientific journal) Publisher：Scientific Reports
© The Author(s) 2017. Despite numerous genetic studies on bone metabolism, understanding of the specific mechanisms is lacking. We developed an efficient screening system to identify novel genes involved in bone metabolism using mutant mouse strains registered with the Exchangeable Gene Trap Clones (EGTC) database. From 1278 trap clones in the EGTC database, 52 candidate lines were selected in the first screening, determined based on "EST profile", "X-gal", "Related article", and "Novel gene". For the second screening, bone morphometric analysis, biomechanical strength analysis, bone X-gal staining, etc. were performed on candidate lines. Forty-two male trap lines (80.8%) showed abnormalities with either bone morphometric analysis or biomechanical strength analysis. In the screening process, X-gal staining was significantly efficient (P = 0.0057). As examples, Lbr and Nedd4 trap lines selected using the screening system showed significant bone decrease and fragility, suggesting a relationship with osteoblast differentiation. This screening system using EGTC mouse lines is extremely efficient for identifying novel genes involved in bone metabolism. The gene trap lines identified as abnormal using this screening approach are highly likely to trap important genes for bone metabolism. These selected trap mice will be valuable for use as novel bio-resources in bone research.
DOI： 10.1038/srep40692
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Roles of the endoplasmic reticulum stress transducer OASIS in fracture healing. Reviewed
Funamoto T, Sekimoto T, Murakami T, Kurogi S, Imaizumi K, Chosa E
Bone 49 ( 4 ) 724 - 32 2011.10
Authorship：Lead author Language：English Publishing type：Research paper (scientific journal)
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COVID-19パンデミックの地域医療代替実習として実施したケアプラン作成実習 Reviewed
舩元 太郎, 安倍 弘生, 宮内 俊一, 齋藤 勝俊, 黒木 純, 中村 佳菜子, 小松 弘幸
医学教育 54 ( 6 ) 607 - 609 2023.12
Authorship：Lead author, Corresponding author Language：Japanese Publishing type：Research paper (scientific journal) Publisher：日本医学教育学会
MISC 【 display / non-display 】
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Anterior apprehension test
舩元 太郎，帖佐 悦男
関節外科 38 ( 5 ) 536 - 537 2019.5
Language：Japanese Publishing type：Article, review, commentary, editorial, etc. (scientific journal) Publisher：メジカルビュー社
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骨粗鬆症地域連携の事例紹介 宮崎大学医学部附属病院の取り組み
舩元 太郎，帖佐 悦男
PROGRESS IN MEDICINE 38 ( 1 ) 19 - 22 2018.1
Language：Japanese Publishing type：Article, review, commentary, editorial, etc. (scientific journal) Publisher：ライフ・サイエンス
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Ⅲ.各種検査法 検体検査 -血液，微生物，関節液など-（共著） Invited Reviewed
舩元太郎, 帖佐悦男
関節外科 35 ( 10 ) 88 - 91 2016.10
Language：Japanese Publishing type：Article, review, commentary, editorial, etc. (trade magazine, newspaper, online media) Publisher：株式会社メジカルビュー社
Presentations 【 display / non-display 】
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当科におけるRA頚椎病変の手術成績の検討
平川 雄介, 黒木 智文, 今里 浩之, 舩元 太郎, 濱中 秀昭, 帖佐 悦男
第63回九州リウマチ学会
Event date： 2022.3.12 - 2022.3.13
Presentation type：Oral presentation (general)
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当科におけるRA頚椎病変の手術成績の検討
平川 雄介, 黒木 智文, 今里 浩之, 舩元 太郎, 濱中 秀昭, 帖佐 悦男
第63回九州リウマチ学会
Event date： 2022.3.12 - 2022.3.13
Presentation type：Oral presentation (general)
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股関節鏡での摘出術後にSurgical dislocationを用いて摘出を行った股関節滑膜性骨軟骨腫症の一例
山元 楓子, 日吉 優, 岩佐 一真, 今里 浩之, 平川 雄介, 山口 洋一朗, 舩元 太郎, 中村 嘉宏, 坂本 武郎, 帖佐 悦男
第142回西日本整形・災害外科学会学術集会
Event date： 2021.12.11 - 2021.12.12
Presentation type：Oral presentation (general)
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診断に時間を要したliosacral screw挿入に伴う上殿動脈仮性動脈瘤の1例
森田 恭史, 坂本 武郎, 中村 嘉宏, 舩元 太郎, 日吉 優, 山口 洋一郎, 今里 浩之, 平川 雄介, 岩佐 一真, 喜多 恒允, 帖佐 悦男
第142回西日本整形・災害外科学会学術集会
Event date： 2021.12.11 - 2021.12.12
Presentation type：Oral presentation (general)
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股関節鏡での摘出術後にSurgical dislocationを用いて摘出を行った股関節滑膜性骨軟骨腫症の一例
山元 楓子, 日吉 優, 岩佐 一真, 今里 浩之, 平川 雄介, 山口 洋一朗, 舩元 太郎, 中村 嘉宏, 坂本 武郎, 帖佐 悦男
第142回西日本整形・災害外科学会学術集会
Event date： 2021.12.11 - 2021.12.12
Presentation type：Oral presentation (general)
Grant-in-Aid for Scientific Research 【 display / non-display 】
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骨系統疾患モデルマウス候補Lbrトラップマウスの表現型解析
2015.04 - 2018.03
科学研究費補助金 基盤研究(C)
Authorship：Principal investigator
Lamin B receptorは重篤な骨系統疾患Greenberg骨異形成症の原因遺伝子と知られている。Lbrトラップマウスの骨表現型の解析を行い、モデルマウスの可能性、およびLBRの骨代謝における働きを研究する。
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明らかな骨量減少をきたすLima1/EPLIN遺伝子欠損マウスの機能解析
2012.04 - 2015.03
科学研究費補助金 基盤研究(C)
Lima1/EPLIN遺伝子欠損マウスの骨強度は低下しており、マイクロCTにて骨構造は疎であった。骨形成能の低下を認め骨芽細胞機能の低下が原因と考えられる。上皮細胞ではLima1/EPLINは細胞骨格の安定化に寄与し、細胞間接着にも関与していることが知られており、骨芽細胞においても類似した機構が想定された。