Details of the Researcher

PHOTO

Michiko Yoshida
Section
Graduate School of Dentistry
Job title
Assistant Professor
Degree

  • 博士（歯学）（東北大学）

Research History 4

  • 2020/10 - Present
    東北大学大学院歯学研究科　地域共生社会歯学講座 顎口腔矯正学分野　助教

  • 2015/05 - 2020/09
    東北大学病院矯正歯科　助教

  • 2014/04 - 2015/03
    日本学術振興会特別研究員 PD

  • 2013/04 - 2014/03
    日本学術振興会特別研究員 DC2

Education 2

  • 東北大学大学院　歯学研究科

    2010/04 - 2014/03

  • Tohoku University　Faculty of Dentistry

    2003/04 - 2009/03

Research Areas 1

  • Life sciences / Developmental dentistry /

Awards 5

  1. 優秀発表賞

    2014/10　日本矯正歯科学会学術大会　転写因子Foxc1はCol10a1の発現誘導を介して内軟骨性骨化を制御する

  2. 2013 ASBMR Young Investigator Travel Grant

    2013/10　The American Society for Bone and Mineral Research　Forkhead protein FoxC1 regulates chondrogenic genes expression by modulating Ihh/Gli2 signaling

  3. 2012 ASBMR Young Investigator Travel Grant

    2012/10　The American Society for Bone and Mineral Research 2012 34th Annual Meetin　The transcription factor FoxC1 regulates chondrogenesis together with Gli2 through induction of PTHrP

  4. 優秀発表賞

    2012/09　日本矯正歯科学会学術大会　転写因子Foxc1はPTHrPの発現誘導を介して内軟骨性骨形成を制御する

  5. 1st Asia-Pacific Bone and Mineral Research Meeting with ANZBMS 22nd Annual Scientific Meeting Travel Award

    2012/07

Papers 15

  1. 開咬症例における歯科矯正用アンカースクリューを用いた矯正歯科治療後戻りの3次元的分析

    小倉 裕樹, 北浦 英樹, 福永 智広, 清流 正弘, 吉田 倫子, 伊藤 新, 大柳 俊仁, 大堀 文俊, 野口 隆弘, 沼崎 研人, 溝口 到

    日本矯正歯科学会大会プログラム・抄録集　83回　233-233　2024/10

    Publisher: (公社)日本矯正歯科学会

  2. Influence of feeding a soft diet on proteoglycan expression in rat temporomandibular joint discs. International-journal

    Kozue Yasuno, Arata Ito, Michiko Yoshida, Tomohiro Fukunaga, Takahiro Honda, Hiroka Tsumaki, Kaya Yamaguchi, Itaru Mizoguchi

    Journal of oral biosciences　2024/06/01

    DOI： 10.1016/j.job.2024.05.009 　

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    OBJECTIVES: Extracellular matrix components play a significant role in maintaining tissue integrity and pathological processes of the temporomandibular joint (TMJ). This study aimed to evaluate the influence of a soft diet on the mRNA expression of proteoglycans and glycosaminoglycans (GAGs) linked to proteoglycan core proteins in rat TMJ discs. METHODS: Thirty 4-week-old male Wistar rats were assigned to one of two groups: a control group fed a regular pellet diet and a soft diet group fed a powdered diet for 4 weeks. The mRNA expression levels of 12 proteoglycans in TMJ discs were evaluated using real-time polymerase chain reaction (PCR). In addition, histomorphometric and biochemical analyses were performed to evaluate the thickness and deoxyribonucleic acid (DNA), GAG, and water content of the TMJ discs. RESULTS: The TMJ disc thickness in the anterior, intermediate, and posterior bands decreased significantly in the soft diet group. The GAG content decreased significantly in the soft-diet group, whereas no significant differences in DNA content or water content ratio were observed between the groups. Real-time PCR indicated that the expression levels of aggrecan, versican, biglycan, decorin, fibromodulin, lumican, and chondroadherin decreased in the soft diet group. The expression levels of all versican isoforms decreased in the soft diet group. CONCLUSIONS: These results indicate that the biomechanical environment of the TMJ caused by a soft diet is closely related to the expression of proteoglycans in TMJ discs, which may eventually increase the fragility of the TMJ discs.

  3. Three-Dimensional Evaluation of Treatment Effects and Post-Treatment Stability of Maxillary Molar Intrusion Using Temporary Anchorage Devices in Open Bite Malocclusion. International-journal

    Hiroki Ogura, Kento Numazaki, Toshihito Oyanagi, Masahiro Seiryu, Arata Ito, Takahiro Noguchi, Fumitoshi Ohori, Michiko Yoshida, Tomohiro Fukunaga, Hideki Kitaura, Itaru Mizoguchi

    Journal of clinical medicine　13　(10)　2024/05/07

    DOI： 10.3390/jcm13102753 　

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    Background: We investigated treatment outcomes and post-treatment stability in 10 patients with an anterior open bite and nonsurgical orthodontics. Methods: The patients underwent maxillary molar intrusion using temporary anchorage devices (TADs) to deepen the overbite due to mandibular autorotation. Lateral cephalograms and dental cast models were obtained before treatment (T0), immediately after it (T1), and >1 year after it (T2). Skeletal and dental cephalometric changes and three-dimensional movements of the maxillary dentitions were evaluated. Results: At T0, cephalometric analysis indicated that patients had skeletal class I with tendencies for a class II jaw relationship and a skeletal open bite. During active treatment (T0 to T1), the maxillary first molar intruded by 1.6 mm, the mandibular first molar extruded by 0.3 mm, the Frankfort-mandibular plane angle decreased by 1.1°, and the overbite increased by 4.1 mm. Statistically significant changes were observed in the amount of vertical movement of the maxillary first molar, Frankfort-mandibular plane angle, and overbite. Three-dimensional (3D) dental cast analysis revealed that the maxillary first and second molars intruded, whereas the anterior teeth extruded, with the second premolar as an infection point. In addition, the maxillary molar was tipped distally by 2.9° and rotated distally by 0.91°. Statistically significant changes were observed in the amount of vertical movement of the central incisor, lateral incisor, canine and first molar, and molar angulation. From T1 to T2, no significant changes in cephalometric measurements or the 3D position of the maxillary dentition were observed. The maxillary and mandibular dentitions did not significantly change during post-treatment follow-up. Conclusions: Maxillary molar intrusion using mini-screws is an effective treatment for open bite correction, with the achieved occlusion demonstrating 3D stability at least 1 year after treatment.

  4. Craniofacial Characteristics and Orthodontic Treatment of Diamond Blackfan Syndrome: Two Case Reports. International-journal

    Satoshi Sasaki, Hideki Kitaura, Maki Goto, Michiko Yoshida, Itaru Mizoguchi

    The Cleft palate-craniofacial journal : official publication of the American Cleft Palate-Craniofacial Association　60　(1)　10556656211053774-10556656211053774　2021/11/17

    DOI： 10.1177/10556656211053774 　

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    Diamond Blackfan anemia (DBA) is a chronic congenital form of erythrocytic hypoplasia in which erythroid precursor cell levels are low. DBA reflects ribosomal dysfunction and is accompanied by hematopoietic cell apoptosis, anemia, and various somatic symptoms. We report the characteristic symptoms of the craniofacial region and the orthodontic treatments of two DBA cases. Case 1 was a 12-year-old female. The typical physical and facial characteristics of DBA were lacking. On initial examination, she exhibited a skeletal Class II jaw and end to end molar relationships and a large overjet. An edgewise appliance was placed after extraction of the first maxillary premolars. After 3 years and 11 months, an appropriate overjet and overbite, rigid intercuspation, and an acceptable profile were evident without any clinical adverse effects. Case 2 was a 13-year-old female. She exhibited a skeletal Class I jaw relationship, a spaced dental arch, the maxillofacial dysplasia characteristic of Binder syndrome, hypoplasia of the right mandibular condyle, and labial protrusions of the maxillary and mandibular incisors. We placed an edgewise appliance and after 1 year and 7 months, the occlusion was optimal in the absence of any adverse effects. Our two DBA cases exhibited a broad spectrum of physical and dentofacial symptoms. Patients with DBA are often prescribed combined steroid/bisphosphonate therapies. Both agents are likely to affect alveolar bone remodeling after tooth extraction and orthodontic tooth movement. Careful consideration of medication with reference to various dentofacial characteristics is necessary.

  5. Ten‐m/Odz3 regulates migration and differentiation of chondrogenic ATDC5 cells via RhoA‐mediated actin reorganization International-journal Peer-reviewed

    Ikuko Takano, Nobuo Takeshita, Michiko Yoshida, Daisuke Seki, Toshihito Oyanagi, Seiji Kimura, Wei Jiang, Kiyo Sasaki, Chisumi Sogi, Masayoshi Kawatsu, Teruko Takano‐Yamamoto

    Journal of Cellular Physiology　236　(4)　2906-2919　2021/04

    Publisher: Wiley

    DOI： 10.1002/jcp.30058 　

    ISSN： 0021-9541

    eISSN： 1097-4652

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    Tenascin-like molecule major (Ten-m)/odd Oz (Odz), a type II transmembrane molecule, is well known to modulate neural development. We have reported that Ten-m/Odz3 is expressed in cartilaginous tissues and cells. Actin cytoskeleton and its regulator ras homolog gene family member A (RhoA) are closely associated with chondrogenesis. The present study aimed to evaluate the function and molecular mechanism of Ten-m/Odz3 during chondrogenesis, focusing on RhoA and the actin cytoskeleton. Ten-m/Odz3 was expressed in precartilaginous condensing mesenchyme in mouse limb buds. Ten-m/Odz3 knockdown in ATDC5 induced actin cytoskeleton reorganization and change of cell shape through modulation of RhoA activity and FGF2 expression. Ten-m/Odz3 knockdown suppressed ATDC5 migration and expression of genes associated with chondrogenesis, such as Sox9 and type II collagen, via RhoA. On the other hand, Ten-m/Odz3 knockdown inhibited proliferation of ATDC5 in a RhoA-independent manner. These findings suggest that Ten-m/Odz3 plays an important role in early chondrogenesis regulating RhoA-mediated actin reorganization.

  6. Dmrt2 promotes transition of endochondral bone formation by linking Sox9 and Runx2 International-journal Peer-reviewed

    Koichiro Ono, Kenji Hata, Eriko Nakamura, Shota Ishihara, Sachi Kobayashi, Masako Nakanishi, Michiko Yoshida, Yoshifumi Takahata, Tomohiko Murakami, Seiichi Takenoshita, Toshihisa Komori, Riko Nishimura, Toshiyuki Yoneda

    Communications Biology　4　(1)　326-326　2021/03

    Publisher: Springer Science and Business Media LLC

    DOI： 10.1038/s42003-021-01848-1 　

    eISSN： 2399-3642

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    <title>Abstract</title>Endochondral bone formation is fundamental for skeletal development. During this process, chondrocytes undergo multiple steps of differentiation and coordinated transition from a proliferating to a hypertrophic stage, which is critical to advance skeletal development. Here, we identified the transcription factor <italic>Dmrt2</italic> (double-sex and mab-3 related transcription factor 2) as a Sox9-inducible gene that promotes chondrocyte hypertrophy in pre-hypertrophic chondrocytes. Epigenetic analysis further demonstrated that Sox9 regulates <italic>Dmrt2</italic> expression through an active enhancer located 18 kb upstream of the <italic>Dmrt2</italic> gene and that this enhancer’s chromatin status is progressively activated through chondrocyte differentiation. <italic>Dmrt2</italic>-knockout mice exhibited a dwarf phenotype with delayed initiation of chondrocyte hypertrophy. Dmrt2 augmented hypertrophic chondrocyte gene expression including <italic>Ihh</italic> through physical and functional interaction with Runx2. Furthermore, Dmrt2 deficiency reduced Runx2-dependent <italic>Ihh</italic> expression. Our findings suggest that Dmrt2 is critical for sequential chondrocyte differentiation during endochondral bone formation and coordinates the transcriptional network between Sox9 and Runx2.

  7. Connective tissue growth factor promotes chemotaxis of preosteoblasts through integrin α5 and Ras during tensile force-induced intramembranous osteogenesis International-journal Peer-reviewed

    Wei Jiang, Nobuo Takeshita, Toshihiro Maeda, Chisumi Sogi, Toshihito Oyanagi, Seiji Kimura, Michiko Yoshida, Kiyo Sasaki, Arata Ito, Teruko Takano-Yamamoto

    Scientific Reports　11　(1)　2368-2368　2021/01

    Publisher: Springer Science and Business Media LLC

    DOI： 10.1038/s41598-021-82246-9 　

    eISSN： 2045-2322

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    <title>Abstract</title>In vertebrates, new bone formation via intramembranous osteogenesis is a critical biological event for development, remodeling, and fracture healing of bones. Chemotaxis of osteoblast lineage cells is an essential cellular process in new bone formation. Connective tissue growth factor (CTGF) is known to exert chemotactic properties on various cells; however, details of CTGF function in the chemotaxis of osteoblast lineage cells and underlying molecular biological mechanisms have not been clarified. The aim of the present study was to evaluate the chemotactic properties of CTGF and its underlying mechanisms during active bone formation through intramembranous osteogenesis. In our mouse tensile force-induced bone formation model, preosteoblasts were aggregated at the osteogenic front of calvarial bones. CTGF was expressed at the osteogenic front, and functional inhibition of CTGF using a neutralizing antibody suppressed the aggregation of preosteoblasts. In vitro experiments using μ-slide chemotaxis chambers showed that a gradient of CTGF induced chemotaxis of preosteoblastic MC3T3-E1 cells, while a neutralizing integrin α5 antibody and a Ras inhibitor inhibited the CTGF-induced chemotaxis of MC3T3-E1 cells. These findings suggest that the CTGF-integrin α5-Ras axis is an essential molecular mechanism to promote chemotaxis of preosteoblasts during new bone formation through intramembranous osteogenesis.

  8. Methionine Enkephalin Suppresses Osteocyte Apoptosis Induced by Compressive Force through Regulation of Nuclear Translocation of NFATc1 Peer-reviewed

    Sogi C, Takeshita N, Jiang W, Kim S, Maeda T, Yoshida M, Oyanagi T, Ito A, Kimura S, Seki D, Takano I, Sakai Y, Fujiwara I, Kure S, Takano-Yamamoto T

    JBMR Plus　4　(7)　2020/07

    Publisher: Wiley

    DOI： 10.1002/jbm4.10369 　

    ISSN： 2473-4039

    eISSN： 2473-4039

  9. Insulin-like growth factor 1 modulates bioengineered tooth morphogenesis. Peer-reviewed

    Oyanagi T, Takeshita N, Hara M, Ikeda E, Chida T, Seki D, Yoshida M, Seiryu M, Takano I, Kimura S, Oshima M, Tsuji T, Takano-Yamamoto T

    Scientific reports　9　(1)　368　2019/01

    DOI： 10.1038/s41598-018-36863-6 　

  10. The transcription factor Foxc1 is necessary for Ihh-Gli2-regulated endochondral ossification Peer-reviewed

    Michiko Yoshida, Kenji Hata, Rikako Takashima, Koichiro Ono, Eriko Nakamura, Yoshifumi Takahata, Tomohiko Murakami, Sachiko Iseki, Teruko Takano-Yamamoto, Riko Nishimura, Toshiyuki Yoneda

    NATURE COMMUNICATIONS　6　6653　2015/03

    DOI： 10.1038/ncomms7653 　

    ISSN： 2041-1723

  11. Regulation of transcriptional network system during bone and cartilage development

    Riko Nishimura, Kenji Hata, Fumiyo Ikeda, Takuma Matsubara, Katsuhiko Amano, Koichiro Ono, Yoko Takigawa, Rikako Takashima, Michiko Yoshida, Eriko Nakamura, Toshiyuki Yoneda

    Journal of Oral Biosciences　57　(4)　165-170　2015

    Publisher: Japanese Association for Oral Biology

    DOI： 10.1016/j.job.2015.06.001 　

    ISSN： 1349-0079

  12. Arid5b facilitates chondrogenesis by recruiting the histone demethylase Phf2 to Sox9-regulated genes Peer-reviewed

    Kenji Hata, Rikako Takashima, Katsuhiko Amano, Koichiro Ono, Masako Nakanishi, Michiko Yoshida, Makoto Wakabayashi, Akio Matsuda, Yoshinobu Maeda, Yutaka Suzuki, Sumio Sugano, Robert H. Whitson, Riko Nishimura, Toshiyuki Yoneda

    Nature Communications　4　2850　2013/11/26

    Publisher: Nature Publishing Group

    DOI： 10.1038/ncomms3850 　

    ISSN： 2041-1723

  13. [Modulation of transcriptional regulation during bone and cartilage development and their disease].

    Riko Nishimura, Kenji Hata, Rikako Takashima, Michiko Yoshida, Eriko Nakamura, Junpei Kida, Hiroko Yagi

    Clinical calcium　23　1585-1593　2013/01/01

    ISSN： 0917-5857

  14. [Role and function regulation of transcription factors in endochondral ossification]. Peer-reviewed

    Nishimura R, Hata K, Takashima R, Yoshida M

    Clinical calcium　22　(5)　643-652　2012/05

    ISSN： 0917-5857

  15. Regulation of endochondral ossification by transcription factors

    Riko Nishimura, Kenji Hata, Koichiro Ono, Rikako Takashima, Michiko Yoshida, Toshiyuki Yoneda

    Journal of Oral Biosciences　54　(4)　180-183　2012

    Publisher: Japanese Association for Oral Biology

    DOI： 10.1016/j.job.2012.09.001 　

    ISSN： 1349-0079

Show all ︎Show first 5

Misc. 26

  1. 軟食摂取が関節円板のproteoglycanのmRNA発現に及ぼす影響

    安野 梢, 吉田倫子, 伊藤 新, 穴田一生, 福永智広, 溝口 到

    第82回日本矯正歯科学会大会プログラム・抄録集　248-248　2023/11

  2. 顎関節円板におけるエラスチンの加齢変化

    伊藤 新, 吉田 倫子, 穴田 一生, 安野 梢, 溝口 到

    第81回日本矯正歯科学会大会プログラム・抄録集　164-164　2022/10

  3. 顎関節荷重負荷がラット関節円板のコラーゲン発現に及ぼす影響

    穴田 一生, 伊藤 新, 安野 梢, 吉田 倫子, 溝口 到

    日本矯正歯科学会大会プログラム・抄録集 80回　146-146　2021/11

  4. 膜性骨化においてCTGFはintegrin α5とRasを介し前駆骨芽細胞のchemotaxisを促す

    竹下 信郎, ジャン・ウェイ, 前田 敏博, 曽木 千純, 大柳 俊仁, 木村 晴地, 吉田 倫子, 佐々木 紀代, 伊藤 新, 山本 照子

    日本矯正歯科学会大会プログラム・抄録集 80回　156-156　2021/11

  5. 牽引力が誘導する膜性骨化においてCTGFはintegrin α5とRasを介して前駆骨芽細胞のchemotaxisを促す

    竹下 信郎, 曽木 千純, 大柳 俊仁, 吉田 倫子, 山本 照子

    日本骨代謝学会学術集会プログラム抄録集 39回　131-131　2021/10

  6. MENKは圧縮力による骨細胞のアポトーシスを抑制する

    曽木千純, 竹下信郎, 伊藤新, 吉田倫子, 大柳俊仁, 藤原幾磨, 山本照子

    日本骨代謝学会学術集会　2019/10

  7. Odz3はRhoA、アクチン制御を介した遊走促進および分化の促進により、ATDC5の軟骨細胞分化を調整する

    高野 郁子, 竹下 信郎, 関 大輔, 大柳 俊仁, 吉田 倫子, 木村 晴地, 川津 正慶, 山本 照子

    日本矯正歯科学会大会プログラム・抄録集　77回　250-250　2018/10

    Publisher: (公社)日本矯正歯科学会

  8. IGF1 regulates morphogenesis of bioengineered teeth via proliferation and differentiation of dental epithelial and mesenchymal cells

    Oyanagi T, Takeshita N, Hara M, Ikeda E, Chida T, Seki D, Yoshida M, Seiryu M, Takano I, Kimura S, Oshima M, Tsuji T, Takano-Yamamoto T

    5th TERMIS World Congress　2018/09

  9. 牽引力負荷された歯根膜の初期反応におけるscleraxisの発現機序と機能の解析

    川津 正慶, 竹下 信郎, 吉田 倫子, 木村 晴地, 清流 正弘, 滝本 晶, 宿南 知佐, 山本 照子

    日本矯正歯科学会大会プログラム・抄録集　76回　193-193　2017/10

    Publisher: (公社)日本矯正歯科学会

  10. 下顎前歯先天性欠如および上顎前歯部に叢生を伴う骨格性I級症例

    吉田 倫子, 清流 正弘, 山本 照子

    日本矯正歯科学会大会プログラム・抄録集　76回　274-274　2017/10

    Publisher: (公社)日本矯正歯科学会

  11. 歯科矯正用アンカースクリューを用いて、上顎前歯欠損部位の閉鎖を行った骨格性下顎前突症例

    吉田 倫子, 清流 正弘, 山本 照子

    東北矯正歯科学会雑誌　24　(1)　68-69　2016/12

    Publisher: 東北矯正歯科学会

    ISSN： 1340-2668

  12. 骨・軟骨分化の制御機構 内軟骨性骨化を制御する転写因子の同定とその分子メカニズムの解明

    波多 賢二, 吉田 倫子, 西村 理行, 米田 俊之

    日本整形外科学会雑誌　90　(8)　S1423-S1423　2016/08

    Publisher: (公社)日本整形外科学会

    ISSN： 0021-5325

  13. IGF1による再生歯の形態制御とそのメカニズム解析

    大柳 俊仁, 竹下 信郎, 関 大輔, 原 真美子, 池田 悦子, 高野 郁子, 清流 正弘, 吉田 倫子, 山本 照子

    日本骨代謝学会学術集会プログラム抄録集　34回　227-227　2016/07

    Publisher: (一社)日本骨代謝学会

    ISSN： 1349-0761

  14. IGF-1を添加した再生歯胚におけるサイズ増大のメカニズムの解析

    大柳 俊仁, 千田 透子, 竹下 信郎, 関 大輔, 高野 郁子, 吉田 倫子, 清流 正弘, 山本 照子

    日本矯正歯科学会大会プログラム・抄録集　74回　208-208　2015/11

    Publisher: (公社)日本矯正歯科学会

  15. 転写因子Foxc1はIhh-Gli2シグナルを促進し内軟骨性骨形成を制御する

    波多 賢二, 吉田 倫子, 中村 恵理子, 高畑 佳史, 村上 智彦, 井関 祥子, 山本 照子, 西村 理行

    Journal of Oral Biosciences Supplement　2015　169-169　2015/09

    Publisher: (一社)歯科基礎医学会

    ISSN： 2187-2333

    eISSN： 2187-9109

  16. 転写因子Zfhx4はOsterixと結合して内軟骨性骨形成の後期過程を制御する

    中村 恵理子, 波多 賢二, 吉田 倫子, 村上 智彦, 高畑 佳史, 阿部 真土, 米田 俊之, 西村 理行

    日本骨代謝学会学術集会プログラム抄録集　33回　162-162　2015/07

    Publisher: (一社)日本骨代謝学会

    ISSN： 1349-0761

  17. 過去10年間に東北大学病院矯正歯科を受診した矯正患者の実態調査

    山本 照子, 後藤 まき, 北浦 英樹, 福永 智広, 竹下 信郎, 清流 正弘, 長谷川 正和, 青沼 智, 金原 正敬, 解良 洋平, 川津 正慶, 加藤 龍史, 木村 桂介, 山田 雅一, 井田 裕人, 佐々木 紀代, 宮下 俊郎, 吉田 倫子, 石田 匡彦, 関 大輔, 高野 郁子, 土江 雄治朗, 則松 佑佳, 坂東 加南

    東北大学歯学雑誌　34　(1)　32-37　2015/06

    Publisher: 東北大学歯学会

    ISSN： 0287-3915

  18. 転写因子Foxc1はIhh-Gli2シグナルを促進し内軟骨性骨形成を制御する

    波多賢二, 吉田倫子, 吉田倫子, 中村恵理子, 高畑佳史, 村上智彦, 井関祥子, 山本照子, 西村理行

    Journal of Oral Biosciences Supplement (Web)　2015　2015

    ISSN： 2187-9109

  19. 転写因子Foxc1はCol10a1の発現誘導を介して内軟骨性骨化を制御する

    吉田 倫子, 波多 賢二, 米田 俊之, 山本 照子

    日本矯正歯科学会大会プログラム・抄録集　73回　207-207　2014/10

    Publisher: (公社)日本矯正歯科学会

  20. The transcription factor Foxc1 controls endochondral ossification through the direct regulation of PTHrP and Col10a1 expression under the partnership with Gli2 and Runx2

    Yoshida M, Hata K, Takashima R, Iseki S, Takano-Yamamoto T, Nishimura R, Yoneda T

    The 41st European Calcified Tissue Society　2014/05

  21. The transcription factor Foxc1 regulates chondrocyte hypertrophy in a synergistic cooperation with Runx2.

    Michiko Yoshida, Kenji Hata, Sachiko Iseki, Teruko Takano-Yamamoto, Riko Nishimura, Toshiyuki Yoneda

    JOURNAL OF BONE AND MINERAL RESEARCH　29　S69-S69　2014/02

    ISSN： 0884-0431

    eISSN： 1523-4681

  22. Forkhead protein FoxC1 regulates chondrogenic genes expression by modulating Ihh/Gli2 signaling

    Yoshida M, Hata K, Takashima R, Iseki S, Takano-Yamamoto T, Nishimura R, Yoneda T

    The American Society for Bone and Mineral Research 2013 35th Annual Meeting　2013/10

  23. 【ストレスによる骨制御】骨および軟骨の発生ならびに疾患における転写制御機構の変動

    西村 理行, 波多 賢二, 高島 利加子, 吉田 倫子, 中村 恵理子, 木田 淳平, 八木 寛子

    Clinical Calcium　23　(11)　1585-1593　2013/10

    Publisher: (株)医薬ジャーナル社

    ISSN： 0917-5857

  24. The transcription factor FoxC1 regulates chondrogenesis together with Gli2 through induction of PTHrP

    Yoshida M, Hata K, Takashima R, Iseki S, Takano-Yamamoto T, Nishimura R, Yoneda T

    2012/10

  25. The transcription factor FoxC1 regulates chondrogenesis together with Gli2 through induction of PTHrP

    Yoshida M, Hata K, Takashima R, Iseki S, Takano-Yamamoto T, Nishimura R, Yoneda T

    Australian & New Zealand Bone & Mineral Society 22nd Annual Scientific Meeting in conjunction with 1st Asia-Pacific Bone and Mineral Research Meeting　2012/09

  26. 転写因子FoxC1はPTHrPを介して内軟骨性骨形成を制御する

    吉田 倫子, 西村 理行, 米田 俊之, 山本 照子

    日本矯正歯科学会大会プログラム・抄録集　71回　172-172　2012/09

    Publisher: (公社)日本矯正歯科学会

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Presentations 4

  1. 学童期における骨格性反対咬合患者への矯正歯科治療 Invited

    吉田倫子

    第35回東北矯正歯科学会大会　2019/05

  2. The transcription factor Foxc1 is necessary for Ihh–Gli2-regulated endochondral ossification

    Yoshida M, Hata K, Takashima R, Ono K, Nakamura E, Takahata Y, Murakami T, Mizoguchi I, Iseki S, Takano-Yamamoto T, Nishimura R, Yoneda T

    2019/03

  3. The transcription factor FoxC1 up-regulates PTHrP expression together with Gli2 in chondrocytes

    2013/05

  4. 転写因子FoxC1はPTHrPの発現誘導を介して内軟骨性骨形成を制御する

    吉田 倫子, 波多 賢二, 高島 利加子, 井関 祥子, 山本 照子, 西村 理行, 米田 俊之

    日本骨代謝学会学術集会　2012/07

Research Projects 5

  1. 歯胚間葉でのFoxc1の機能と分子制御解明-iPS細胞を用いた歯胚発生への応用-

    吉田 倫子

    Offer Organization: 日本学術振興会

    System: 科学研究費助成事業 若手研究

    Category: 若手研究

    Institution: 東北大学

    2020/04 - 2023/03

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    常染色体優性遺伝性疾患Axenfeld-Rieger症候群（ARS）は、緑内障や無虹彩など眼の異常を主症状とし、その他に歯の先天欠如や矮小歯・タウロドント歯などの歯の形態異常が認められる。ARSの原因遺伝子としてFoxc1が知られている。そのため、Foxc1の遺伝子異常が、ARSにおける歯の発生異常を誘導すると推察されるが、歯の発生におけるFoxc1の発現、機能、および分子制御は不明である。代表者は、過去にFoxc1がヘッジホッグのシグナル伝達分子Gli2と物理的に結合し、PTHrPの発現を促すことにより、内軟骨性骨化を制御することを見出した。加えて、マウス初代軟骨細胞において、Foxc1によるPTHrP発現制御にエピジェネティクスが関与することを明らかにした。さらに、Gli2の異常により矮小歯や癒合歯を呈し、歯の発生過程における形態および位置異常が認められることが知られている。これらの知見から代表者は、歯性細胞で発現するFoxc1がGli2と相互関係を持ち、正常な歯の発生に寄与すると仮説を立てた。一方、代表者が所属するグループは、マウスiPS細胞由来歯性細胞の樹立に成功したが、この細胞を用いた歯胚発生には至っていない。そこで、本研究の目的は、歯の発生過程における歯性細胞でのFoxc1の機能と分子メカニズムを解明し、得られる知見に基づいて、Foxc1をiPS細胞から歯胚発生能をもつ歯性細胞の樹立に応用することである。本研究により、未だ全容の明らかでない先天性の歯の発生異常の病因解明につながることが期待されるとともに、歯の再生に必要なiPS細胞由来の細胞シーズの獲得実現が期待される。本年度は、昨年度に引き続きマウス歯胚の歯性細胞におけるFoxc1の機能解析を行った。野生型マウスの臼歯歯胚から歯性細胞を単離し、この細胞にFoxc1の過剰発現・ノックダウンを行い、歯性間葉細胞マーカーや象牙芽細胞マーカーの発現解析、BrdU染色とTUNEL染色による増殖とアポトーシスの解析を行った。

  2. Roles of methionine enkephalin produced by osteocytes in mechanical stress-induced bone metabolism

    Takeshita Nobuo

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research

    Category: Grant-in-Aid for Scientific Research (C)

    Institution: Tohoku University

    2018/04/01 - 2021/03/31

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    Mechanical stimuli induce osteocyte apoptosis, followed by bone resorption. A neural factor, methionine enkephalin (MENK), is involved in bone metabolism and apoptosis. In this study, we clarified the role of MENK in the osteocyte apoptosis promoted by mechanical stimuli. Our data showed that MENK expression was reduced by compressive force loading on the parietal bones, and that this reduction in MENK expression was regulated by CCN2/CTGF. In addition, the apoptosis of osteocytes induced by compressive force was suppressed by MENK through the regulation of calcium signaling and NFATc1 nuclear translocation.

  3. Hif1αの役割解明に基づくiPS細胞由来歯性上皮細胞への新規分化誘導方法の確立 Competitive

    吉田倫子

    Offer Organization: 日本学術振興会

    System: 科学研究費助成事業 基盤研究(C)

    2017/04 - 2020/03

  4. IGF-Iによる再生歯胚の形態制御機構に関する研究 Competitive

    吉田倫子

    Offer Organization: 日本学術振興会

    System: 科学研究費助成事業 若手研究(B)

    2015/04 - 2017/03

  5. 顎顔面発育過程における転写因子Foxc1の役割と作用機序の解明 Competitive

    吉田倫子

    Offer Organization: 日本学術振興会

    System: 科学研究費助成事業 特別研究員奨励費(PD)

    2013/04 - 2015/03