2024/07/28 更新

お知らせ

 

写真a

キュウモト ユカリ
久本 由香里
KYUMOTO YUKARI
所属
歯学研究院 歯学部門 助教
歯学部 歯学科(併任)
歯学府 口腔科学専攻(併任)
歯学府 歯学専攻(併任)
職名
助教
連絡先
メールアドレス
電話番号
0926426302
プロフィール
<研究活動> ・破骨細胞の細胞融合に関する研究 ・糖尿病関連因子と骨代謝 <教育活動> ・学部学生への解剖学実習補助 ・大学院生への研究指導
外部リンク

学位

  • 博士(薬学)

研究テーマ・研究キーワード

  • 研究テーマ: 破骨細胞由来生理活性物質を介した骨-脂肪コミュニケーションと肥満・糖代謝制御

    研究キーワード: 破骨細胞、脂肪細胞、糖代謝

    研究期間: 2016年4月

  • 研究テーマ: 糖尿病誘発因子RBP4による骨破壊制御

    研究キーワード: 破骨細胞、骨破壊、糖尿病

    研究期間: 2014年9月 - 2016年3月

  • 研究テーマ: Tim-3/Galectin-9システムによる骨破壊制御メカニズム解明

    研究キーワード: 破骨細胞 骨吸収

    研究期間: 2014年2月

  • 研究テーマ: 破骨細胞と異物巨細胞の比較と破骨細胞の融合のみに特化した分子の検索

    研究キーワード: 破骨細胞 骨吸収 異物巨細胞 細胞融合

    研究期間: 2014年2月

論文

  • Extremely High Expression of Antisense RNA for Wilms' Tumor 1 in Active Osteoclasts: Suppression of Wilms' Tumor 1 Protein Expression during Osteoclastogenesis. 査読 国際誌

    Li YJ., Kukita A., Kyumoto-Nakamura Y., Kukita T.

    186 ( 9 )   2317 - 25   2016年9月

     詳細を見る

    記述言語:日本語   掲載種別:研究論文(学術雑誌)  

    Extremely High Expression of Antisense RNA for Wilms' Tumor 1 in Active Osteoclasts: Suppression of Wilms' Tumor 1 Protein Expression during Osteoclastogenesis.
    Wilms' tumor 1 (WT1), a zinc-finger transcription regulator of the early growth response family, identified as the product of a tumor suppressor gene of Wilms' tumors, bears potential ability to induce macrophage differentiation in blood cell differentiation. Herein, we examined the involvement of WT1 in the regulation of osteoclastogenesis. We detected a high level of WT1 protein expression in osteoclast precursors; however, WT1 expression was markedly suppressed during osteoclastogenesis. We examined expression of WT1 transcripts in bone tissue by RNA in situ hybridization. We found a high level of antisense transcripts in osteoclasts actively resorbing bone in mandible of newborn rats. Expression of antisense WT1 RNA in mandible was also confirmed by Northern blot analysis and strand-specific RT-PCR. Overexpression of antisense WT1 RNA in RAW-D cells, an osteoclast precursor cell line, resulted in a marked enhancement of osteoclastogenesis, suggesting that antisense WT1 RNA functions to suppress expression of WT1 protein in osteoclastogenesis. High level expression of antisense WT1 RNA may contribute to commitment to osteoclastogenesis, and may allow osteoclasts to maintain or stabilize their differentiation state.

    DOI: 10.1016/j.ajpath.2016.05.005

  • Growth differentiation factor-5 promotes brown adipogenesis in systemic energy expenditure. 査読 国際誌

    Hinoi E., Nakamura Y., Takada S., Fujita H., Iezaki T., Hashizume S., Takahashi S., Odaka Y., Watanabe T., Yoneda Y.

    Diabetes   63 ( 1 )   162 - 175   2014年1月

     詳細を見る

    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Although growth differentiation factor-5 (GDF5) has been implicated in skeletal development and joint morphogenesis in mammals, little is known about its functionality in adipogenesis and energy homeostasis. Here, we show a critical role of GDF5 in regulating brown adipogenesis for systemic energy expenditure in mice. GDF5 expression was preferentially upregulated in brown adipose tissues from inborn and acquired obesity mice. Transgenic overexpression of GDF5 in adipose tissues led to a lean phenotype and reduced susceptibility to diet-induced obesity through increased systemic energy expenditure. Overexpression of GDF5 facilitated the development of brown fat-like cells, called brite or beige cells, along with the expression of uncoupling protein-1 in inguinal subcutaneous white adipose tissue. In mutant mice harboring the dominant-negative GDF5, marked impairment in energy expenditure and thermogenesis was seen under obesogenic conditions. Recombinant GDF5 promoted brown adipogenesis through the mothers against decapentaplegic homolog (Smad) and peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) pathways after activation of bone morphogenetic protein receptor (BMPR). These results suggest that brown adipogenesis and energy homeostasis are both positively regulated by the GDF5/BMPR/Smad/PGC-1α signaling pathway in adipose tissues. Modulation of these pathways might be an effective therapeutic strategy for obesity and type 2 diabetes.

    DOI: 10.2337/db13-0808

  • Repression of adipogenesis through promotion of Wnt/ß-catenin signaling by TIS7 up-regulated in adipocytes under hypoxia. 査読 国際誌

    Nakamura Y.*, Hinoi E.*, Iezaki T., Takada S., Hashizume S., Takahata Y., Tsuruta E., Takahashi S., Yoneda Y.

    BBA Mol. Basis Dis.   1832 ( 8 )   1117 - 1128   2013年8月

     詳細を見る

    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Although tetradecanoyl phorbol acetate induced sequence-7 (TIS7) has been identified as a co-activator/repressor of gene transcription in different eukaryotic cells, little attention has been paid to the functionality of TIS7 in adipocytes. Here, we evaluated the possible role of TIS7 in mechanisms underlying the regulation of adipogenesis. TIS7 expression was preferentially up-regulated in white adipose tissues (WAT) of obesity model mice as well as in pre-adipocytic 3T3-L1 cells cultured under hypoxic conditions. TIS7 promoter activity was selectively enhanced by activating transcription factor-6 (ATF6) among different transcription factors tested, while induction of TIS7 by hypoxic stress was markedly prevented by knockdown of ATF6 by shRNA in 3T3-L1 cells. Overexpression of TIS7 markedly inhibited Oil Red O staining and expression of particular adipogenic genes in 3T3-L1 cells. TIS7 synergistically promoted gene transactivation mediated by Wingless-type mouse mammary tumor virus integration site family (Wnt)/β-catenin, while blockade of the Wnt/β-catenin pathway by a dominant negative form of T-cell factor-4 (DN-TCF4) markedly prevented the inhibition of adipogenesis in 3T3-L1 cells with TIS7 overexpression. TIS7 predominantly interacted with β-catenin in the nucleus of WAT in the genetically obese ob/ob mice as well as in 3T3-L1 cells cultured under hypoxic conditions. Both knockdown of TIS7 by shRNA and introduction of DN-TCF4 similarly reversed the hypoxia-induced inhibition of adipogenic gene expression in 3T3-L1 cells. These findings suggest that TIS7 could play a pivotal role in adipogenesis through interacting with β-catenin to promote the canonical Wnt signaling in pre-adipocytes under hypoxic stress such as obesity.

    DOI: 10.1016/j.bbadis.2013.03.010

  • Osteoclastogenesis is negatively regulated by D-serine produced by osteoblasts. 査読 国際誌

    Takarada T., Takarada-Iemata M., Takahata Y., Yamada D., Yamamoto T., Nakamura Y., Hinoi E., Yoneda Y.

    J. Cell. Physiol.   227   3477 - 3487   2012年10月

     詳細を見る

    記述言語:英語  

  • Positive regulation by GABA(B) receptor subunit-1 of chondrogenesis through acceleration of nuclear translocation of activating transcription factor-4. 査読 国際誌

    Takahata Y., Hinoi E., Takarada T., Nakamura Y., Ogawa S., Yoneda Y.

    J. Biol. Chem.   287   33293 - 33303   2012年9月

     詳細を見る

    記述言語:英語  

  • Negative regulation of osteoblastogenesis through downregulation of runt-related transcription factor-2 in osteoblastic MC3T3-E1 cells with stable overexpression of the cystine/glutamate antiporter xCT subunit. 査読 国際誌

    Uno K., Takarada T., Takarada-Iemata M., Nakamura Y., Fujita H., Hinoi E., Yoneda Y.

    J. Cell. Physiol.   226   2953 - 2964   2011年11月

     詳細を見る

    記述言語:英語  

  • Osteoblastic GABAB receptors negatively regulate osteoblastogenesis toward disturbance of osteoclastogenesis mediated by receptor activator of nuclear factor-kB ligand in mouse bone. 査読 国際誌

    Takahata Y., Takarada T., Hinoi E., Nakamura Y., Fujita H., Yoneda Y.

    J. Biol. Chem.   286   32906 - 32917   2011年9月

     詳細を見る

    記述言語:英語  

  • Glutamate preferentially suppresses osteoblastogenesis than adipogenesis through the cystine/glutamate antiporter in mesenchymal stem cells. 査読 国際誌

    Takarada-Iemata M., Takarada T., Nakamura Y. Nakatani E., Hori O., Yoneda Y.

    J. Cell. Physiol.   226   652 - 665   2011年3月

     詳細を見る

    記述言語:英語  

  • Positive regulation by GABABR1 subunit of leptin expression through gene transactivation in adipocytes. 査読 国際誌

    Nakamura Y.*, Hinoi E.*, Takarada T., Takahata Y., Yamamoto T., Fujita H., Takada S., Hashizume S., Yoneda Y.

    PLoS ONE.   6   e20167   2011年3月

     詳細を見る

    記述言語:英語  

  • A negative correlation between expression profiles of runt-related transcription factor-2 and cystine/glutamate antiporter xCT subunit in ovariectomized mouse bone. 査読 国際誌

    Uno K., Takarada T., Nakamura Y., Fujita H., Hinoi E., Yoneda Y.

    J. Pharmacol. Sci.   115   309 - 319   2011年2月

     詳細を見る

    記述言語:英語  

  • Predominant promotion by tacrolimus of chondrogenic differentiation to proliferating chondrocytes. 査読 国際誌

    Nakamura Y.*, Takarada T.*, Kodama A., Hinoi E., Yoneda Y.

    J. Pharmacol. Sci.   109   413 - 423   2009年3月

     詳細を見る

    記述言語:英語  

  • Differential regulation of cellular maturation in chondrocytes and osteoblasts by glycine. 査読 国際誌

    Takahata Y., Takarada T., Osawa M., Hinoi E., Nakamura Y., Yoneda Y.

    Cell Tissue Res.   333   91 - 103   2008年7月

     詳細を見る

    記述言語:英語  

  • Erythropoietin receptor signal is crucial for periodontal ligament stem cell-based tissue reconstruction in periodontal disease. 査読 国際誌

    Mhd Fouad Zakaria, Soichiro Sonoda, Hiroki Kato, Lan Ma, Norihisa Uehara, Yukari Kyumoto-Nakamura, M Majd Sharifa, Liting Yu, Lisha Dai, Erika Yamauchi-Tomoda, Reona Aijima, Haruyoshi Yamaza, Fusanori Nishimura, Takayoshi Yamaza

    Scientific reports   14 ( 1 )   6719 - 6719   2024年3月

     詳細を見る

    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Alveolar bone loss caused by periodontal disease eventually leads to tooth loss. Periodontal ligament stem cells (PDLSCs) are the tissue-specific cells for maintaining and repairing the periodontal ligament, cementum, and alveolar bone. Here, we investigated the role of erythropoietin receptor (EPOR), which regulates the microenvironment-modulating function of mesenchymal stem cells, in PDLSC-based periodontal therapy. We isolated PDLSCs from patients with chronic periodontal disease and healthy donors, referred to as PD-PDLSCs and Cont-PDLSCs, respectively. PD-PDLSCs exhibited reduced potency of periodontal tissue regeneration and lower expression of EPOR compared to Cont-PDLSCs. EPOR-silencing suppressed the potency of Cont-PDLSCs mimicking PD-PDLSCs, whereas EPO-mediated EPOR activation rejuvenated the reduced potency of PD-PDLSCs. Furthermore, we locally transplanted EPOR-silenced and EPOR-activated PDLSCs into the gingiva around the teeth of ligament-induced periodontitis model mice and demonstrated that EPOR in PDLSCs participated in the regeneration of the periodontal ligament, cementum, and alveolar bone in the ligated teeth. The EPOR-mediated paracrine function of PDLSCs maintains periodontal immune suppression and bone metabolic balance via osteoclasts and osteoblasts in the periodontitis model mice. Taken together, these results suggest that EPOR signaling is crucial for PDLSC-based periodontal regeneration and paves the way for the development of novel options for periodontal therapy.

    DOI: 10.1038/s41598-024-57361-y

    リポジトリ公開URL: https://hdl.handle.net/2324/7178660

  • miR-92a-3p encapsulated in bone metastatic mammary tumor cell–derived extracellular vesicles modulates mature osteoclast longevity 招待 査読 国際誌

    Norihisa Uehara, Yukari Kyumoto-Nakamura, Yoshikazu Mikami, Manabu Hayatsu, Soichiro Sonoda, Takayoshi Yamaza, Akiko Kukita, Toshio Kukita

    Cancer Science   2022年12月

     詳細を見る

    記述言語:英語   掲載種別:研究論文(学術雑誌)  

  • In vitro and in vivo detection of tunneling nanotubes in normal and pathological osteoclastogenesis involving osteoclast fusion 査読 国際誌

    Jing-Qi Zhang, Akira Takahashi, Jiong-Yan Gu, Xiaoxu Zhang, Yukari Kyumoto-Nakamura, Akiko Kukita, Norihisa Uehara, Hidenobu Hiura, Takayoshi Yamaza, Toshio Kukita

    Laboratory Investigation   101 ( 12 )   1571 - 1584   2021年12月

     詳細を見る

    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Osteoclasts are multinucleated cells formed through specific recognition and fusion of mononuclear osteoclast precursors derived from hematopoietic stem cells. Detailed cellular events concerning cell fusion in osteoclast differentiation remain ambiguous. Tunneling nanotubes (TNTs), actin-based membrane structures, play an important role in intercellular communication between cells. We have previously reported the presence of TNTs in the fusion process of osteoclastogenesis. Here we analyzed morphological details of TNTs using scanning electron microscopy. The osteoclast precursor cell line RAW-D was stimulated to form osteoclast-like cells, and morphological details in the appearance of TNTs were extensively analyzed. Osteoclast-like cells could be classified into three types; early osteoclast precursors, late osteoclast precursors, and multinucleated osteoclast-like cells based on the morphological characteristics. TNTs were frequently observed among these three types of cells. TNTs could be classified into thin, medium, and thick TNTs based on the diameter and length. The shapes of TNTs were dynamically changed from thin to thick. Among them, medium TNTs were often observed between two remote cells, in which side branches attached to the culture substrates and beaded bulge-like structures were often observed. Cell-cell interaction through TNTs contributed to cell migration and rapid transport of information between cells. TNTs were shown to be involved in cell-cell fusion between osteoclast precursors and multinucleated osteoclast-like cells, in which movement of membrane vesicles and nuclei was observed. Formation of TNTs was also confirmed in primary cultures of osteoclasts. Furthermore, we have successfully detected TNTs formed between osteoclasts observed in the bone destruction sites of arthritic rats. Thus, formation of TNTs may be important for the differentiation of osteoclasts both in vitro and in vivo. TNTs could be one target cellular structure for the regulation of osteoclast differentiation and function in bone diseases.

    DOI: 10.1038/s41374-021-00656-9

  • Modulation of osteoclastogenesis through adrenomedullin receptors on osteoclast precursors: initiation of differentiation by asymmetric cell division 査読 国際誌

    Toshio Kukita, Hidenobu Hiura, Jiong-Yan Gu, Jing-Qi Zhang, Yukari Kyumoto-Nakamura, Norihisa Uehara, Sara Murata, Soichiro Sonoda, Takayoshi Yamaza, Ichiro Takahashi, Akiko Kukita

    Laboratory Investigation   101 ( 11 )   1449 - 1457   2021年11月

     詳細を見る

    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Adrenomedullin (ADM), a member of the calcitonin family of peptides, is a potent vasodilator and was shown to have the ability to modulate bone metabolism. We have previously found a unique cell surface antigen (Kat1 antigen) expressed in rat osteoclasts, which is involved in the functional regulation of the calcitonin receptor (CTR). Cross-linking of cell surface Kat1 antigen with anti-Kat1 antigen monoclonal antibody (mAbKat1) stimulated osteoclast formation only under conditions suppressed by calcitonin. Here, we found that ADM provoked a significant stimulation in osteoclastogenesis only in the presence of calcitonin; a similar biological effect was seen with mAbKat1 in the bone marrow culture system. This stimulatory effect on osteoclastogenesis mediated by ADM was abolished by the addition of mAbKat1. 125I-labeled rat ADM (125I-ADM)-binding experiments involving micro-autoradiographic studies demonstrated that mononuclear precursors of osteoclasts abundantly expressed ADM receptors, and the specific binding of 125I-ADM was markedly inhibited by the addition of mAbKat1, suggesting a close relationship between the Kat1 antigen and the functional ADM receptors expressed on cells in the osteoclast lineage. ADM receptors were also detected in the osteoclast progenitor cells in the late mitotic phase, in which only one daughter cell of the dividing cell express ADM receptors, suggesting the semiconservative cell division of the osteoclast progenitors in the initiation of osteoclastogenesis. Messenger RNAs for the receptor activity-modifying-protein 1 (RAMP1) and calcitonin receptor-like receptor (CRLR) were expressed in cells in the osteoclast lineage; however, the expression of RAMP2 or RAMP3 was not detected in these cells. It is suggested that the Kat1 antigen is involved in the functional ADM receptor distinct from the general ADM receptor, consisting of CRLR and RAMP2 or RAMP3. Modulation of osteoclastogenesis through functional ADM receptors abundantly expressed on mononuclear osteoclast precursors is supposed to be important in the fine regulation of osteoclast differentiation in a specific osteotrophic hormonal condition with a high level of calcitonin in blood.

    DOI: 10.1038/s41374-021-00633-2

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

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

    The Journal of Immunology   206 ( 12 )   3053 - 3063   2021年6月

     詳細を見る

    記述言語:その他   掲載種別:研究論文(学術雑誌)  

    Systemic transplantation of stem cells from human exfoliated deciduous teeth (SHED) is used to treat systemic lupus erythematosus (SLE)-like disorders in MRL/lpr mice. However, the mechanisms underlying the SHED-based therapy remain unclear. In this study, we hypothesized that trophic factors within SHED-releasing extracellular vesicles (SHED-EVs) ameliorate the SLE-like phenotypes in MRL/lpr mice. SHED-EVs were isolated from the culture supernatant of SHED. SHED-EVs were treated with or without RNase and systemically administered to MRL/lpr mice. Subsequently, recipient bone marrow mesenchymal stem cells (BMMSCs) isolated from SHED-EV-administered MRL/lpr mice were examined for the in vitro and in vivo activity of hematopoietic niche formation and immunoregulation. Furthermore, the recipient BMMSCs were secondarily transplanted into MRL/lpr mice. The systemic SHED-EV infusion ameliorated the SLE-like phenotypes in MRL/lpr mice and improved the functions of recipient BMMSCs by rescuing Tert mRNA-associated telomerase activity, hematopoietic niche formation, and immunoregulation. The secondary transplantation of recipient BMMSCs recovered the immune condition and renal functions of MRL/lpr mice. The RNase treatment depleted RNAs, such as microRNAs, within SHED-EVs, and the RNA-depleted SHED-EVs attenuated the benefits of SHED-EVs in MRL/lpr mice. Collectively, our findings suggest that SHED-secreted RNAs, such as microRNAs, play a crucial role in treating SLE by targeting the telomerase activity of recipient BMMSCs.

    DOI: 10.4049/jimmunol.2001312

  • Extracellular vesicles from deciduous pulp stem cells recover bone loss by regulating telomerase activity in an osteoporosis mouse model 査読 国際誌

    Soichiro Sonoda, Sara Murata, Kento Nishida, Hiroki Kato, Norihisa Uehara, Yukari N. Kyumoto, Haruyoshi Yamaza, Ichiro Takahashi, Toshio Kukita, Takayoshi Yamaza

    Stem Cell Research & Therapy   11 ( 1 )   296 - 296   2020年12月

     詳細を見る

    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Abstract

    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

  • 破骨細胞機能制御に関連する新規破骨細胞特異的膜表面抗原

    顧 炯炎, 久本 由香里, 寺町 順平, 日浦 秀暢, 張 旌旗, 張 暁旭, 上原 範久, 山座 孝義, 久木田 明子, 久木田 敏夫

    Journal of Oral Biosciences Supplement   2020   205 - 205   2020年9月

     詳細を見る

    記述言語:日本語  

  • Characteristics of differentiation of osteoclast cells irradiated with active species in atmospheric oxygen plasma 査読

    Nobuya Hayashi, Yuki Inoue, Yukari Kyumoto, Toshio Kukita

    JAPANESE JOURNAL OF APPLIED PHYSICS   59   2020年6月

     詳細を見る

    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Variations in osteoclast cell number are observed when osteoclast precursor cells are irradiated with atmospheric dielectric barrier discharge plasma. Active species generated by the oxygen plasma control the differentiation function of the osteoclast precursor cells. Long-lifetime active species such as H2O2 and NOx- dissolved in the culture medium decrease the osteoclast number due to the inactivation of the differentiation function of the osteoclast precursor cells. When short-lifetime active species such as O* and OH* make contact with the osteoclast precursor cells directly, the osteoclast number tends to increase. Short-lifetime active species induce the enhancement of the gene expression of NFATc1. (C) 2020 The Japan Society of Applied Physics

    DOI: 10.35848/1347-4065/ab7ba9

  • Acetylsalicylic Acid Treatment and Suppressive Regulation of AKT Accelerate Odontogenic Differentiation of Stem Cells from the Apical Papilla 査読

    Yosuke Tanaka, Soichiro Sonoda, Haruyoshi Yamaza, Sara Murata, Kento Nishida, Yukari Kyumoto-Nakamura, Norihisa Uehara, Kazuaki Nonaka, Toshio Kukita, Takayoshi Yamaza

    Journal of Endodontics   45 ( 5 )   591 - 598.e6   2019年5月

     詳細を見る

    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Introduction: Stem cells isolated from the root apical papilla of human teeth (stem cells from the apical papilla [SCAPs])are capable of forming tooth root dentin and are a feasible source for bioengineered tooth root regeneration. In this study, we examined the effect of acetylsalicylic acid (ASA)on odontogenic differentiation of SCAPs in vitro and in vivo. Methods: SCAPs were cultured under odontogenic conditions supplemented with or without ASA. ASA-treated SCAPs were also subcutaneously transplanted into immunocompromised mice. Results: ASA accelerates in vitro and in vivo odontogenic differentiation of SCAPs associated with down-regulation of runt-related nuclear factor 2 and up-regulation of specificity protein 7, nuclear factor I C, and dentin phosphoprotein. ASA up-regulated the phosphorylation of AKT in the odontogenic SCAPs. Of interest, pretreatments with phosphoinositide 3-kinase inhibitor LY294402 and small interfering RNA for AKT promoted ASA-induced in vitro and in vivo odontogenic differentiation of SCAPs. LY294402 and small interfering RNA for AKT also suppressed the ASA-induced expression of runt-related nuclear factor 2 and enhanced ASA-induced expression of specificity protein 7, nuclear factor I C, and dentin phosphoprotein in SCAPs. Conclusions: These findings suggest that a combination of ASA treatment and suppressive regulation of the phosphoinositide 3-kinase–AKT signaling pathway is a novel approach for SCAP-based tooth root regeneration.

    DOI: 10.1016/j.joen.2019.01.016

  • Osteoblast lineage-specific cell-surface antigen (A7) regulates osteoclast recruitment and calcification during bone remodeling 査読

    Tamer Badawy, Yukari Kyumoto-Nakamura, Norihisa Uehara, Jingqi Zhang, Soichiro Sonoda, Hidenobu Hiura, Takayoshi Yamaza, Akiko Kukita, Toshio Kukita

    Laboratory Investigation   99 ( 6 )   866 - 884   2019年1月

     詳細を見る

    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Bone remodeling is a continuous process characterized by highly coordinated cell-cell interactions in distinct multi-cellular units. Osteoclasts, which are specialized bone resorbing cells, play a central role in bone remodeling. Although the RANKL/RANK axis determines the gross number of osteoclasts present in bone tissue, detailed molecular events regulating bone remodeling related to osteoclast recruitment, initiation of bone remodeling, and coupling of bone resorption and bone formation are still ambiguous. We hypothesized that osteoblast-specific cell-surface molecules contribute to the molecular modulation of bone remodeling. Therefore, we searched for regulatory cell-surface molecules expressed on osteoblasts by use of B-cell hybridoma technology. We obtained a monoclonal antibody A7 (A7 MAb) highly specific to cells of osteoblast-lineage. Here we describe the expression pattern and possible role of A7 antigen specifically recognized by A7 MAb. In vitro, A7 antigen was expressed on cell-surface of osteoblasts and osteoblast-like bone marrow stromal cells. In vivo, A7 antigen was detected in a subset of bone surface osteoblasts and in osteocytes, with a typical cell membrane expression pattern. Tissue array analysis showed only a limited expression of A7 antigen in osteocytes close to the bone surface. Immunoblotting and immunoprecipitation analysis showed that A7 antigen is a lineage-specific cell-surface protein with an approximate molecular weight of 45 KDa. Cross-linking of cell-surface A7 antigen in cultures of osteoclastogenesis showed stimulation of osteoclast formation. Marked suppression of calcification in primary osteoblast cultures was observed when A7 antigen was cross-linked with anti-A7 antigen MAb, A7 MAb. These data suggest that A7 antigen regulates recruitment of osteoclasts and triggering of calcification. A7 antigen may be an important molecule involved in the precise regulation of bone remodeling.

    DOI: 10.1038/s41374-018-0179-4

  • Suppression of AKT-mTOR signal pathway enhances osteogenic/dentinogenic capacity of stem cells from apical papilla 査読

    Yosuke Tanaka, Soichiro Sonoda, Haruyoshi Yamaza, Sara Murata, Kento Nishida, Shion Hama, Yukari Kyumoto-Nakamura, Norihisa Uehara, Kazuaki Nonaka, Toshio Kukita, Takayoshi Yamaza

    Stem Cell Research and Therapy   9 ( 1 )   2018年11月

     詳細を見る

    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Background: Stem cells from apical papilla (SCAP) are a subpopulation of mesenchymal stem cells (MSCs) isolated from the apical papilla of the developing tooth root apex of human teeth. Because of their osteogenic/dentinogenic capacity, SCAP are considered as a source for bone and dentin regeneration. However, little is understood about the molecular mechanism of osteogenic/dentinogenic differentiation of SCAP. Phosphoinositide 3 kinase (PI3K)-AKT-mammalian target of rapamycin (mTOR) signal pathway participates in regulating the differentiation of various cell types, such as MSCs. In this study, we examined the role of the PI3K-AKT-mTOR signal pathway in the osteogenic/dentinogenic differentiation of SCAP. Moreover, we challenge to fabricate scaffold-free SCAP-based spheroidal calcified constructs. Methods: SCAP were pretreated with or without small interfering RNA for AKT (AKT siRNA), PI3K inhibitor LY294402, and mTOR inhibitor rapamycin and were cultured under osteogenic/dentinogenic differentiation to examine in vitro and in vivo calcified tissue formation. Moreover, SCAP-based cell aggregates were pretreated with or without LY294402 and rapamycin. The cell aggregates were cultured under osteogenic/dentinogenic condition and were analyzed the calcification of the aggregates. Results: Pretreatment with AKT siRNA, LY294402, and rapamycin enhances the in vitro and in vivo calcified tissue-forming capacity of SCAP. SCAP were fabricated as scaffold-free spheroids and were induced into forming calcified 3D constructs. The calcified density of the spheroidal constructs was enhanced when the spheroids were pretreated with LY294402 and rapamycin. Conclusions: Our findings indicate that the suppression of PI3K-AKT-mTOR signal pathway plays a role in not only enhancing the in vivo and in vitro osteogenic/dentinogenic differentiation of SCAP, but also promoting the calcification of scaffold-free SCAP-based calcified constructs. These findings suggest that a suppressive regulation of PI3K-AKT-mTOR signal pathway is a novel approach for SCAP-based bone and dentin regeneration.

    DOI: 10.1186/s13287-018-1077-9

  • Unique Osteoblast-Specific Cell-Surface Antigen Useful for Odondoblast Ontology and Dentin Regeneration 招待 査読 国際誌

    Tamer Badawy, Yukari Kyumoto-Nakamura, Norihisa Uehara, Jingqi Zhang, Hidenobu Hiura, Soichiro Sonoda, Takayoshi Yamaza, Akiko Kukita, Toshio Kukita

    International Journal of Oral Health & Dental Management   2 ( 2 )   1 - 7   2018年6月

     詳細を見る

    記述言語:日本語   掲載種別:研究論文(学術雑誌)  

    Unique Osteoblast-Specific Cell-Surface Antigen Useful for Odontoblast Ontology and Dentin Regeneration

    DOI: 10.33425/2639-9490.1018

  • Exogenous nitric oxide stimulates the odontogenic differentiation of rat dental pulp stem cells 招待 査読 国際誌

    Sonoda S., Mei Y. F., Atsuta I., Danjo A., Yamaza H., Hama S., Nishida K., Tang R., Kyumoto-Nakamura Y., Uehara N., Kukita T., Nishimura F., Yamaza T.

    SCIENTIFIC REPORTS   8 ( 1 )   2018年2月

     詳細を見る

    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Nitric oxide (NO) is thought to play a pivotal regulatory role in dental pulp tissues under both physiological and pathological conditions. However, little is known about the NO functions in dental pulp stem cells (DPSCs). We examined the direct actions of a spontaneous NO gas-releasing donor, NOC-18, on the odontogenic capacity of rat DPSCs (rDPSCs). In the presence of NOC-18, rDPSCs were transformed into odontoblast-like cells with long cytoplasmic processes and a polarized nucleus. NOC-18 treatment increased alkaline phosphatase activity and enhanced dentin-like mineralized tissue formation and the expression levels of several odontoblast-specific genes, such as runt related factor 2, dentin matrix protein 1 and dentin sialophosphoprotein, in rDPSCs. In contrast, carboxy-PTIO, a NO scavenger, completely suppressed the odontogenic capacity of rDPSCs. This NO-promoted odontogenic differentiation was activated by tumor necrosis factor-NF-κB axis in rDPSCs. Further in vivo study demonstrated that NOC-18-application in a tooth cavity accelerated tertiary dentin formation, which was associated with early nitrotyrosine expression in the dental pulp tissues beneath the cavity. Taken together, the present findings indicate that exogenous NO directly induces the odontogenic capacity of rDPSCs, suggesting that NO donors might offer a novel host DPSC-targeting alternative to current pulp capping agents in endodontics.

    DOI: 10.1038/s41598-018-21183-6

  • IL-1β Induces Pathologically Activated Osteoclasts Bearing Extremely High Levels of Resorbing Activity: A Possible Pathological Subpopulation of Osteoclasts, Accompanied by Suppressed Expression of Kindlin-3 and Talin-1 招待 査読 国際誌

    Takuma Shiratori, Yukari Kyumoto-Nakamura, Akiko Kukita, Norihisa Uehara, Jingqi Zhang, Kinuko Koda, Mako Kamiya, Tamer Badawy, Erika Tomoda, Xianghe Xu, Takayoshi Yamaza, Yasuteru Urano, Kiyoshi Koyano and Toshio Kukita

    The Journal of Immunology   200 ( 1 )   218 - 228   2018年1月

     詳細を見る

    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DOI: 10.4049/jimmunol.1602035

  • Osteoblast-derived Laminin-332 is a novel negative regulator of osteoclastogenesis in bone microenvironments 招待 査読 国際誌

    Uehara N., Kukita A., Kyumoto-Nakamura Y., Yamaza T., Yasuda H., Kukita T.

    LABORATORY INVESTIGATION   97 ( 10 )   1235 - 1244   2017年10月

     詳細を見る

    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Laminin-332 (Lm-332), a major basement membrane protein, has been shown to provide a niche for some stem cells. Here, we found that Lm-332 was expressed in osteoblasts, and is implicated in the regulation of osteoclast differentiation. Immunofluorescence analysis of laminin-β3, a unique component of Lm-332, indicated specific expression of laminin-β3 in osteoblast-like cells localized on bone surface. RT-PCR analysis confirmed that α3, β3, and γ2 chains of Lm-332 were all expressed in primary osteoblasts prepared from mouse calvaria. Lm-332 markedly inhibited osteoclastogenesis induced by receptor activator of nuclear factor kappa B (NF-κB) ligand (RANKL) when bone marrow-derived macrophages (BMMs) were cultured on Lm-332-coated plates. Lm-332 also blocked RANKL-induced activation of mitogen-activated protein kinases (MAPKs) (ERK, JNK, and p38) and expression of NFATc1, c-Fos, and c-Jun. Lm-332 suppressed osteoclast differentiation while retaining macrophage phenotypes, including nonspecific esterase activity and gene expression of lysozyme and EGF-like module-containing mucin-like hormone receptor-like 1 (Emr1). Furthermore, the treatment of primary osteoblasts with osteoclastogenic factors dramatically suppressed expression of Lm-332. These findings suggest that Lm-332 produced by osteoblasts in bone tissues has a pivotal role in controlling normal bone remodeling through suppressing osteoclastogenesis.

    DOI: 10.1038/labinvest.2017.55

    リポジトリ公開URL: https://hdl.handle.net/2324/7173558

  • The transcriptional modulator Ifrd1 controls PGC-1α expression under short-term adrenergic stimulation in brown adipocytes. 査読 国際誌

    Park G., Horie T., Kanayama T., Fukasawa K., Iezaki T., Onishi Y., Ozaki K., Nakamura Y., Yoneda Y., Takarada T., Hinoi E.

    284 ( 5 )   784 - 795   2017年3月

     詳細を見る

    記述言語:日本語   掲載種別:研究論文(学術雑誌)  

    The transcriptional modulator Ifrd1 controls PGC-1α expression under short-term adrenergic stimulation in brown adipocytes.
    Sympathetic tone activates the function of classical brown adipocytes, which constitutively exist in the brown adipose tissue (BAT), and inducible brown adipocytes (so-called beige adipocytes), which sporadically reside within the white adipose tissue (WAT). Here we identified the transcriptional modulator interferon-related developmental regulator 1 (Ifrd1) as a negative regulator of thermogenic and mitochondrial gene expression in brown adipocytes. Ifrd1 expression was markedly induced by cold exposure and administration of CL-316243 (a β3 adrenergic agonist) in interscapular brown adipose and inguinal subcutaneous WATs, but not in epididymal visceral WAT, in vivo. Adrenergic stimulation also induced Ifrd1 expression in brown adipocytes in a cAMP responsive element binding protein-dependent manner in vitro. CL-316243 injection markedly elevated thermogenic and mitochondrial gene expression, including peroxisome proliferator-activated receptor γ coactivator 1α (Pgc1a) in the subcutaneous WAT of Ifrd1 knockout mice compared with gene expression in wild-type mice. Pgc1a promoter activity enhanced by the transcription factor specificity protein 1 (Sp1) was markedly repressed by co-introduction of Ifrd1 in brown adipocytes, whereas the repression was markedly prevented by the addition of trichostatin A, a histone deacetylase inhibitor. Moreover, adrenergic stimulation induced complex formation between Ifrd1, Sp1 and mSIN3B, which is a component of the SIN complex containing histone deacetylase, in brown adipocytes. These findings, therefore, suggest that Ifrd1 could be a pivotal negative regulator of sympathetic regulation of thermogenic and mitochondrial gene expression in brown adipocytes by interacting with Sp1 and the mSIN3 complex.

    DOI: 10.1111/febs.14019

  • Transcriptional Modulator Ifrd1 Regulates Osteoclast Differentiation through Enhancing the NF-κB/NFATc1 Pathway. 国際誌

    Takashi Iezaki, Kazuya Fukasawa, Gyujin Park, Tetsuhiro Horie, Takashi Kanayama, Kakeru Ozaki, Yuki Onishi, Yoshifumi Takahata, Yukari Nakamura, Takeshi Takarada, Yukio Yoneda, Takashi Nakamura, Jean Vacher, Eiichi Hinoi

    Molecular and cellular biology   36 ( 19 )   2451 - 63   2016年10月

     詳細を見る

    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Bone homeostasis is maintained by the synergistic actions of bone-resorbing osteoclasts and bone-forming osteoblasts. Here, we show that the transcriptional coactivator/repressor interferon-related developmental regulator 1 (Ifrd1) is expressed in osteoclast lineages and represents a component of the machinery that regulates bone homeostasis. Ifrd1 expression was transcriptionally regulated in preosteoclasts by receptor activator of nuclear factor κB (NF-κB) ligand (RANKL) through activator protein 1. Global deletion of murine Ifrd1 increased bone formation and decreased bone resorption, leading to a higher bone mass. Deletion of Ifrd1 in osteoclast precursors prevented RANKL-induced bone loss, although no bone loss was observed under normal physiological conditions. RANKL-dependent osteoclastogenesis was impaired in vitro in Ifrd1-deleted bone marrow macrophages (BMMs). Ifrd1 deficiency increased the acetylation of p65 at residues K122 and K123 via the inhibition of histone deacetylase-dependent deacetylation in BMMs. This repressed the NF-κB-dependent transcription of nuclear factor of activated T cells, cytoplasmic 1 (NFATc1), an essential regulator of osteoclastogenesis. These findings suggest that an Ifrd1/NF-κB/NFATc1 axis plays a pivotal role in bone remodeling in vivo and represents a therapeutic target for bone diseases.

    DOI: 10.1128/MCB.01075-15

    リポジトリ公開URL: https://hdl.handle.net/2324/7178661

  • Transcriptional Modulator Ifrd1 Regulates Osteoclast Differentiation through Enhancing the NF-κB/NFATc1 Pathway. 査読 国際誌

    Iezaki T., Fukasawa K., Park G., Horie T., Kanayama T., Ozaki K., Onishi Y., Takahata Y., Nakamura Y., Takarada T., Yoneda Y., Nakamura T., Vacher J., Hinoi E.

    2016年9月

     詳細を見る

    記述言語:日本語  

  • The Transcriptional Modulator Interferon-Related Developmental Regulator 1 in Osteoblasts Suppresses Bone Formation and Promotes Bone Resorption. 査読 国際誌

    Iezaki T., Onishi Y., Ozaki K., Fukasawa K., Takahata Y., Nakamura Y., Fujikawa K., Takarada T., Yoneda Y., Yamashita Y., Shioi G., Hinoi E.

    31 ( 3 )   573 - 584   2016年3月

     詳細を見る

    記述言語:日本語   掲載種別:研究論文(学術雑誌)  

    The Transcriptional Modulator Interferon-Related Developmental Regulator 1 in Osteoblasts Suppresses Bone Formation and Promotes Bone Resorption.
    Bone homeostasis is maintained by the synergistic actions of bone-resorbing osteoclasts and bone-forming osteoblasts. Although interferon-related developmental regulator 1 (Ifrd1) has been identified as a transcriptional coactivator/repressor in various cells, little attention has been paid to its role in osteoblastogenesis and bone homeostasis thus far. Here, we show that Ifrd1 is a critical mediator of both the cell-autonomous regulation of osteoblastogenesis and osteoblast-dependent regulation of osteoclastogenesis. Osteoblast-specific deletion of murine Ifrd1 increased bone formation and decreased bone resorption, causing high bone mass. Ifrd1 deficiency enhanced osteoblast differentiation and maturation along with increased expression of Runx2 and osterix (Osx). Mechanistically, Ifrd1 deficiency increased the acetylation status of p65, a component of NF-κB, at residues K122 and K123 via the attenuation of the interaction between p65 and histone deacetylase (HDAC). This led to the nuclear export of p65 and a decrease in NF-κB-dependent Smad7 expression and the subsequent enhancement of Smad1/Smad5/Smad8-dependent transcription. Moreover, a high bone mass phenotype in the osteoblast-specific deletion of Ifrd1 was markedly rescued by the introduction of one Osx-floxed allele but not of Runx2-floxed allele. Coculture experiments revealed that Ifrd1-deficient osteoblasts have a higher osteoprotegerin (OPG) expression and a lower ability to support osteoclastogenesis. Ifrd1 deficiency attenuated the interaction between β-catenin and HDAC, subsequently increasing the acetylation of β-catenin at K49, leading to its nuclear accumulation and the activation of the β-catenin-dependent transcription of OPG. Collectively, the expression of Ifrd1 in osteoblasts repressed osteoblastogenesis and activated osteoclastogenesis through modulating the NF-κB/Smad/Osx and β-catenin/OPG pathways, respectively. These findings suggest that Ifrd1 has a pivotal role in bone homeostasis through its expression in osteoblasts in vivo and represents a therapeutic target for bone diseases.

    DOI: 10.1002/jbmr.2720

▼全件表示

講演・口頭発表等

  • Galectin-9による破骨細胞分化制御メカニズムの解明:NFATc1の発現を抑制する転写因子MafB及びIRF-8の関与

    久本 由香里, 上原 範久, 久木田 明子, 久木田 敏夫

    第33回日本骨代謝学会学術集会  2015年7月 

     詳細を見る

    開催年月日: 2015年7月

    記述言語:日本語   会議種別:シンポジウム・ワークショップ パネル(公募)  

    開催地:新宿   国名:日本国  

  • 転写制御因子Ifrd1による脂肪細胞分化の調節

    中村 由香里, 檜井 栄一, 米田幸雄

    日本薬学会北陸支部第125回例会 

     詳細を見る

    開催年月日: 2013年11月

    記述言語:その他   会議種別:口頭発表(一般)  

    開催地:金沢   国名:その他  

  • 転写制御因子Ifrd1による脂肪細胞分化抑制機構

    中村 由香里, 檜井 栄一, 米田幸雄

    第122回日本薬理学会近畿部会 

     詳細を見る

    開催年月日: 2012年11月

    記述言語:その他   会議種別:口頭発表(一般)  

    開催地:大阪   国名:その他  

  • Ifrd1による脂肪細胞分化制御機構

    中村 由香里, 檜井 栄一, 米田幸雄

    次世代を担う創薬・医療薬理シンポジウム2012 

     詳細を見る

    開催年月日: 2012年9月

    記述言語:その他   会議種別:口頭発表(一般)  

    開催地:神戸   国名:その他  

  • 脂肪細胞分化調節機構における転写制御因子Ifrd1の役割

    中村 由香里, 檜井 栄一, 米田幸雄

    生体機能と創薬シンポジウム2012 

     詳細を見る

    開催年月日: 2012年8月

    記述言語:その他   会議種別:シンポジウム・ワークショップ パネル(公募)  

    開催地:神戸   国名:その他  

  • 脂肪細胞における転写因子Ifrd1の機能

    中村 由香里, 檜井 栄一, 米田幸雄

    第121回日本薬理学会近畿部会 

     詳細を見る

    開催年月日: 2012年6月

    記述言語:その他   会議種別:口頭発表(一般)  

    開催地:徳島   国名:その他  

  • GABABR1サブユニットによる脂肪細胞のleptin発現調節

    中村 由香里, 檜井 栄一, 宝田 剛志, 高畑 佳史, 米田 幸雄

    日本薬学会北陸支部第123回例会 

     詳細を見る

    開催年月日: 2011年11月

    記述言語:その他   会議種別:口頭発表(一般)  

    開催地:金沢   国名:その他  

  • Positive regulation by GABABR1 subunit of leptin expression through gene transactivation in adipocytes

    中村 由香里, 檜井 栄一, 宝田 剛志, 山本 朋未, 高田 紗矢, 米田 幸雄

    日本分子生物学会第11回春季シンポジウム ・ 金沢国際がん生物シンポジウム 

     詳細を見る

    開催年月日: 2011年5月

    記述言語:その他   会議種別:シンポジウム・ワークショップ パネル(公募)  

    開催地:金沢   国名:その他  

  • 転写因子Ifrd1の脂肪細胞における発現

    中村 由香里, 檜井 栄一, 高田 紗矢, 宝田 剛志, 米田 幸雄

    第118回日本薬理学会近畿部会 

     詳細を見る

    開催年月日: 2010年11月

    記述言語:その他   会議種別:口頭発表(一般)  

    開催地:大阪   国名:その他  

  • GABABR1サブユニットによる脂肪細胞のleptin発現制御

    中村 由香里, 宝田 剛志, 檜井 栄一, 米田 幸雄

    第117回日本薬理学会近畿部会 

     詳細を見る

    開催年月日: 2010年7月

    記述言語:その他   会議種別:口頭発表(一般)  

    開催地:徳島   国名:その他  

  • 脂肪細胞分化におけるGABABレセプターの調節機能

    中村 由香里, 宝田 剛志, 檜井 栄一, 米田 幸雄

    日本薬学会第130年会 

     詳細を見る

    開催年月日: 2010年3月

    記述言語:その他   会議種別:シンポジウム・ワークショップ パネル(公募)  

    開催地:岡山   国名:その他  

  • GABABR1サブユニット欠損マウスにおける脂肪分化調節

    中村 由香里, 宝田 剛志, 檜井 栄一, 米田 幸雄

    第83回日本薬理学会年会 

     詳細を見る

    開催年月日: 2010年3月

    記述言語:その他   会議種別:シンポジウム・ワークショップ パネル(公募)  

    開催地:大阪   国名:その他  

  • 脂肪細胞におけるGABABR1サブユニットの機能

    中村 由香里, 宝田 剛志, 檜井 栄一, 米田 幸雄

    第116回日本薬理学会近畿部会 

     詳細を見る

    開催年月日: 2009年11月

    記述言語:その他   会議種別:口頭発表(一般)  

    開催地:滋賀   国名:その他  

  • Down-regulation of glutamate transporter expression by lipopolysaccharide in cultured astrocytes. 国際会議

    Nakamura, Y., Ogura, M., Taniura, H., Nakamichi, N. and Yoneda, Y.

    The 22nd Biennial Meeting of the ISN/APSN Joint Meeting 

     詳細を見る

    開催年月日: 2009年8月

    記述言語:その他   会議種別:シンポジウム・ワークショップ パネル(公募)  

    開催地:釜山   国名:大韓民国  

  • FK506による増殖期軟骨細胞分化の促進

    中村 由香里, 宝田 剛志, 米田 幸雄

    第27回日本骨代謝学会学術集会 

     詳細を見る

    開催年月日: 2009年7月

    記述言語:その他   会議種別:シンポジウム・ワークショップ パネル(公募)  

    開催地:大阪   国名:その他  

  • 脂肪細胞に発現するGABAシグナル分子

    中村 由香里, 宝田 剛志, 米田 幸雄

    日本薬学会第129年会 

     詳細を見る

    開催年月日: 2009年3月

    記述言語:その他   会議種別:シンポジウム・ワークショップ パネル(公募)  

    開催地:京都   国名:その他  

  • 根尖歯乳頭組織由来幹細胞に発現する転写因子PITX2の機能解析

    久本 由香里、園田 聡一朗、加藤 大樹、上原 範久、山座 孝義

    2023年9月 

     詳細を見る

    開催年月日: 2023年9月

    記述言語:日本語  

    開催地:東京   国名:日本国  

  • Galectin-9/Tim-3シグナルを介した破骨細胞分化制御メカニズムの解明

    久本 由香里, 上原 範久, 久木田 明子, 山座 孝義, 久木田 敏夫

    第42回日本分子生物学会年会  2019年12月 

     詳細を見る

    開催年月日: 2019年12月

    記述言語:日本語   会議種別:シンポジウム・ワークショップ パネル(公募)  

    開催地:福岡   国名:日本国  

  • 破骨細胞分化制御におけるGalectin-9/Tim-3シグナルの関与

    久本 由香里, 上原 範久, 久木田 明子, 久木田 敏夫

    第36回 日本骨代謝学会学術集会  2018年7月 

     詳細を見る

    開催年月日: 2018年7月

    記述言語:日本語  

    開催地:長崎   国名:日本国  

  • Galectin-9による破骨細胞分化抑制因子MafBの発現制御

    久本 由香里, 上原 範久, 久木田 明子, 山座 孝義, 久木田 敏夫

    第58回 歯科基礎医学会  2016年8月 

     詳細を見る

    開催年月日: 2016年8月

    記述言語:日本語  

    開催地:札幌   国名:日本国  

  • Galectin-9による破骨細胞分化抑制と転写因子MafBの発現制御メカニズムの解明

    久本 由香里, 上原 範久, 久木田 明子, 久木田 敏夫

    第34回 日本骨代謝学会学術集会  2016年7月 

     詳細を見る

    開催年月日: 2016年7月

    記述言語:日本語  

    開催地:大阪   国名:日本国  

  • Galectin-9による破骨細胞形成抑制機構:MafB制御系関与の可能性

    久本 由香里, 上原 範久, 久木田 明子, 久木田 敏夫

    第57回歯科基礎医学会学術大会  2015年9月 

     詳細を見る

    開催年月日: 2015年9月 - 2016年9月

    記述言語:日本語  

    開催地:新潟   国名:日本国  

  • ラミニン-332によるRANK発現調節とマクロファージ-破骨細胞分化転換の制御

    久本 由香里, 上原 範久, 久木田 明子, 保田 尚孝, 久木田 敏夫

    第33回日本骨代謝学会学術集会  2015年7月 

     詳細を見る

    開催年月日: 2015年7月

    記述言語:日本語   会議種別:シンポジウム・ワークショップ パネル(公募)  

    国名:日本国  

  • 細胞外マトリックス分子ラミニン332の破骨細胞形成抑制作用

    久本 由香里, 上原 範久, 久木田 明子, 保田 尚孝, 久木田 敏夫

    第14回 西日本骨・関節関連疾患懇話会  2015年7月 

     詳細を見る

    開催年月日: 2015年7月

    記述言語:日本語   会議種別:口頭発表(一般)  

    開催地:九州大学   国名:日本国  

  • 免疫制御膜表面分子Tim-3を介する炎症性骨破壊制御

    森山 加奈子, 久木田 明子, 上原 範久, 久本 由香里, 髙橋 一郎, 久木田 敏夫

    第32回日本骨代謝学会学術集会  2014年7月 

     詳細を見る

    開催年月日: 2014年7月

    記述言語:日本語   会議種別:口頭発表(一般)  

    開催地:大阪   国名:日本国  

  • 免疫調節膜表面分子Tim-3を介した炎症性骨破壊の効果的制御

    森山 加奈子, 久木田 明子, 上原 範久, 張 旌旗, 久本 由香里, 髙橋 一郎, 久木田 敏夫

    第13回西日本骨・関節関連疾患懇話会  2014年7月 

     詳細を見る

    開催年月日: 2014年7月

    記述言語:日本語   会議種別:口頭発表(一般)  

    開催地:九州大学   国名:日本国  

  • GABABR1サブユニット分子による破骨細胞分化の調節

    高畑 佳史, 宝田 剛志, 中村 由香里, 檜井 栄一, 米田 幸雄

    第119回日本薬理学会近畿部会 

     詳細を見る

    開催年月日: 2011年7月

    記述言語:その他   会議種別:口頭発表(一般)  

    開催地:名古屋   国名:その他  

  • GABABR1サブユニット安定発現骨芽細胞株の機能解析

    高畑 佳史, 宝田 剛志, 中村 由香里, 米田 幸雄

    第27回日本骨代謝学会学術集会 

     詳細を見る

    開催年月日: 2009年7月

    記述言語:その他   会議種別:シンポジウム・ワークショップ パネル(公募)  

    開催地:大阪   国名:その他  

  • 免疫調節分子Tim-3の破骨細胞での発現と炎症性骨破壊制御

    森山 加奈子, 久木田 明子, 上原 範久, 久本 由香里, 髙橋 一郎, 久木田 敏夫

    第56回歯科基礎医学会 

     詳細を見る

    記述言語:日本語   会議種別:口頭発表(一般)  

    開催地:福岡   国名:日本国  

  • Osteoclasts Formed under Stimulation by IL-1β Possess Extremely High Ability to Secrete Protons and to Resorb Dentin with Abnormal Adhesiveness, Imaged by pH-Sensitive Fluorescence Probes 国際会議

    Takuma Shiratori, Akiko Kukita, Yukari Kyumoto-Nakamura, Norihisa Uehara, Jingqi Zhang, Kinuko Koda, Mako Kamiya, Tamer Badawy, Xianghe Xu, Takayoshi Yamaza, Yasuteru Urano, Kiyoshi Koyano, Toshio Kukita

    American Society for Bone and Mineral Research 2017 Annual Meeting  2017年9月 

     詳細を見る

    記述言語:英語  

    国名:アメリカ合衆国  

▼全件表示

産業財産権

特許権   出願件数: 1件   登録件数: 1件
実用新案権   出願件数: 0件   登録件数: 0件
意匠権   出願件数: 0件   登録件数: 0件
商標権   出願件数: 0件   登録件数: 0件

所属学協会

  • 日本骨代謝学会

  • 歯科基礎医学会

  • 日本解剖学会

共同研究・競争的資金等の研究課題

  • 病的活性化破骨細胞の骨吸収能亢進メカニズムの解明

    2022年

    出産・育児復帰者支援

      詳細を見る

    担当区分:研究代表者  資金種別:学内資金・基金等

  • 糖尿病誘発因子を標的とした新規骨破壊制御法の開発に関する研究

    研究課題/領域番号:21K16933  2021年 - 2023年

    日本学術振興会  科学研究費助成事業  若手研究

      詳細を見る

    担当区分:研究代表者  資金種別:科研費

  • 病的活性化破骨細胞に発現する膜表面分子を標的とした病的骨破壊特異的制御法の開発

    研究課題/領域番号:19K24098  2019年 - 2020年

    日本学術振興会  科学研究費助成事業  研究活動スタート支援

      詳細を見る

    担当区分:研究代表者  資金種別:科研費

  • 破骨細胞由来生理活性物質を介した骨-脂肪コミュニケーションと肥満・糖代謝制御

    研究課題/領域番号:16K20413  2016年 - 2017年

    科学研究費助成事業  若手研究(B)

      詳細を見る

    担当区分:研究代表者  資金種別:科研費

  • 糖尿病誘発因子RBP4による骨破壊制御

    研究課題/領域番号:26893194  2014年 - 2015年

    科学研究費助成事業  若手研究(スタートアップ)

      詳細を見る

    担当区分:研究代表者  資金種別:科研費

  • 転写調節因子Ifrd1を標的とする生活習慣病の新規薬物治療法開発

    研究課題/領域番号:24 2846  2012年 - 2013年

    日本学術振興会  科学研究費助成事業  特別研究員奨励費

      詳細を見る

    担当区分:研究代表者  資金種別:科研費

▼全件表示

教育活動概要

  • 解剖学、解剖学実習、発生学、口腔組織学、口腔解剖学
    大学院生への研究指導

担当授業科目

  • 解剖学実習2

    2024年12月 - 2025年2月   冬学期

  • 解剖学実習1

    2024年10月 - 2024年12月   秋学期

  • 解剖学2

    2024年6月 - 2024年8月   夏学期

  • 解剖学1

    2024年4月 - 2024年6月   春学期

  • 解剖学実習2

    2023年12月 - 2024年2月   冬学期

  • 解剖学実習1

    2023年10月 - 2023年12月   秋学期

  • 解剖学2

    2023年6月 - 2023年8月   夏学期

  • 解剖学1

    2023年4月 - 2023年6月   春学期

  • 発生学

    2023年4月 - 2023年6月   春学期

  • 解剖学実習2

    2022年12月 - 2023年2月   冬学期

  • 解剖学実習1

    2022年10月 - 2022年12月   秋学期

  • 口腔組織学1

    2022年6月 - 2022年8月   夏学期

  • 解剖学2

    2022年6月 - 2022年8月   夏学期

  • 口腔解剖学

    2022年4月 - 2022年9月   前期

  • 発生学

    2022年4月 - 2022年6月   春学期

  • 解剖学1

    2022年4月 - 2022年6月   春学期

  • 口腔組織学Ⅱ

    2021年10月 - 2022年3月   後期

  • 解剖学

    2021年4月 - 2022年3月   通年

  • 解剖学

    2020年4月 - 2021年3月   通年

  • 硬組織研究法

    2020年4月 - 2021年3月   通年

  • 発生学

    2020年4月 - 2020年9月   前期

  • 分子口腔解剖学

    2019年4月 - 2020年3月   通年

  • 解剖学

    2019年4月 - 2020年3月   通年

  • 硬組織研究法

    2019年4月 - 2020年3月   通年

  • 発生学

    2019年4月 - 2019年9月   前期

  • 分子口腔解剖学

    2018年4月 - 2019年3月   通年

  • 解剖学

    2018年4月 - 2019年3月   通年

  • 硬組織研究法

    2018年4月 - 2019年3月   通年

  • 発生学

    2018年4月 - 2018年9月   前期

  • 解剖学

    2017年4月 - 2018年3月   通年

  • 分子口腔解剖学

    2017年4月 - 2018年3月   通年

  • 硬組織研究法

    2017年4月 - 2018年3月   通年

  • 発生学

    2017年4月 - 2017年9月   前期

  • 解剖学

    2016年4月 - 2017年3月   通年

  • 硬組織研究法

    2016年4月 - 2017年3月   通年

  • 分子口腔解剖学

    2016年4月 - 2017年3月   通年

  • 発生学

    2016年4月 - 2016年9月   前期

  • 解剖学

    2015年4月 - 2016年3月   通年

  • 分子口腔解剖学

    2015年4月 - 2016年3月   通年

  • 硬組織研究法

    2015年4月 - 2016年3月   通年

  • 基幹教育セミナー

    2015年4月 - 2015年9月   前期

  • 分子口腔解剖学演習

    2014年4月 - 2015年3月   通年

  • 解剖学

    2014年4月 - 2015年3月   通年

  • 分子口腔解剖学

    2014年4月 - 2015年3月   通年

  • 硬組織研究法

    2014年4月 - 2014年9月   前期

  • 口腔組織学Ⅱ

    2014年4月 - 2014年9月   前期

  • 口腔細胞生物学

    2014年4月 - 2014年9月   前期

▼全件表示

FD参加状況

  • 2019年9月   役割:参加   名称: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〜

    主催組織:部局

  • 2017年10月   役割:参加   名称:第2回4部局合同男女共同参画FD

    主催組織:部局

  • 2015年9月   役割:参加   名称:科学研究費改革の方向性、歯学教育の現状と課題

    主催組織:部局

  • 2015年3月   役割:参加   名称:基幹教育セミナーのためのFD研修会

    主催組織:全学

  • 2014年9月   役割:参加   名称:科研費獲得のポイント

    主催組織:部局

  • 2014年8月   役割:参加   名称:新GPA制度実施のためのFD

    主催組織:全学

  • 2014年4月   役割:参加   名称:第1回全学FD

    主催組織:全学

▼全件表示

メディア報道

  • 「やせる脂肪」ともいわれる褐色脂肪細胞の分化を促進するある特定のサイトカインを確認した。 このサイトカインは、メタボリック症候群対策など、肥満を予防する新たな医薬品の開発などに活用が期待される。 新聞・雑誌

    北國新聞  2011年6月

     詳細を見る

    「やせる脂肪」ともいわれる褐色脂肪細胞の分化を促進するある特定のサイトカインを確認した。
    このサイトカインは、メタボリック症候群対策など、肥満を予防する新たな医薬品の開発などに活用が期待される。