Details of the Researcher

PHOTO

Tetsuhiro Kajikawa
Section
Tohoku University Hospital
Job title
Senior Assistant Professor
Degree

  • 博士（歯学）（大阪大学）

Research History 5

  • 2021/09 - Present
    東北大学 大学院歯学研究科 エコロジー歯学講座 歯内歯周治療学分野 講師

  • 2019/01 - 2021/08
    University of Pennsylvania School of Dental Medicine, Research Associate

  • 2015/04 - 2019/09
    National Institute of Dental and Craniofacial Research, Oral Immunity and Infection Unit, Special Volunteer

  • 2014/04 - 2018/12
    University of Pennsylvania School of Dental Medicine, Postdoctoral Fellow

  • 2011/04 - 2014/03
    大阪大学 歯学部附属病院 医員

Education 2

  • 大阪大学大学院歯学研究科

    2007/04 - 2011/03

  • 大阪大学歯学部

    2000/04 - 2006/03

Professional Memberships 2

  • 日本歯科保存学会

  • 日本歯周病学会

Research Interests 5

  • Neutrophils

  • T cell

  • Immunology

  • Molecular biology

  • Periodontology

Research Areas 3

  • Life sciences / Molecular biology /

  • Life sciences / Immunology /

  • Life sciences / Conservative dentistry and endodontics /

Awards 5

  1. JADR / Lotte Award

    2024/11　The Japanese Association for Dental Research (JADR)

  2. 第6回 口腔医科学フロンティア研究会 奨励賞

    2024/05

  3. 2019 PDM Research Day Award for Poster Presentation

    2019/05

  4. 10th International Workshop on Complement Therapeutics, Travel award

    2017/06

  5. 大阪大学歯学会 優秀研究奨励賞

    2013/07

Papers 43

  1. Mice Lacking PLAP-1/Asporin Show Alteration of Periodontal Ligament Structures and Acceleration of Bone Loss in Periodontitis Peer-reviewed

    Masaki Kinoshita, Satoru Yamada, Junichi Sasaki, Shigeki Suzuki, Tetsuhiro Kajikawa, Tomoaki Iwayama, Chiharu Fujihara, Satoshi Imazato, Shinya Murakami

    International Journal of Molecular Sciences　24　(21)　15989-15989　2023/11/05

    Publisher: MDPI AG

    DOI： 10.3390/ijms242115989 　

    eISSN： 1422-0067

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    Periodontal ligament-associated protein 1 (PLAP-1), also known as Asporin, is an extracellular matrix protein expressed in the periodontal ligament and plays a crucial role in periodontal tissue homeostasis. Our previous research demonstrated that PLAP-1 may inhibit TLR2/4-mediated inflammatory responses, thereby exerting a protective function against periodontitis. However, the precise roles of PLAP-1 in the periodontal ligament (PDL) and its relationship to periodontitis have not been fully explored. In this study, we employed PLAP-1 knockout mice to investigate its roles and contributions to PDL tissue and function in a ligature-induced periodontitis model. Mandibular bone samples were collected from 10-week-old male C57BL/6 (WT) and PLAP-1 knockout (KO) mice. These samples were analyzed through micro-computed tomography (μCT) scanning, hematoxylin and eosin (HE) staining, picrosirius red staining, and fluorescence immunostaining using antibodies targeting extracellular matrix proteins. Additionally, the structure of the PDL collagen fibrils was examined using transmission electron microscopy (TEM). We also conducted tooth extraction and ligature-induced periodontitis models using both wild-type and PLAP-1 KO mice. PLAP-1 KO mice did not exhibit any changes in alveolar bone resorption up to the age of 10 weeks, but they did display an enlarged PDL space, as confirmed by μCT and histological analyses. Fluorescence immunostaining revealed increased expression of extracellular matrix proteins, including Col3, BGN, and DCN, in the PDL tissues of PLAP-1 KO mice. TEM analysis demonstrated an increase in collagen diameter within the PDL of PLAP-1 KO mice. In line with these findings, the maximum stress required for tooth extraction was significantly lower in PLAP-1 KO mice in the tooth extraction model compared to WT mice (13.89 N ± 1.34 and 16.51 N ± 1.31, respectively). In the ligature-induced periodontitis model, PLAP-1 knockout resulted in highly severe alveolar bone resorption, with a higher number of collagen fiber bundle tears and significantly more osteoclasts in the periodontium. Our results demonstrate that mice lacking PLAP-1/Asporin show alteration of periodontal ligament structures and acceleration of bone loss in periodontitis. This underscores the significant role of PLAP-1 in maintaining collagen fibrils in the PDL and suggests the potential of PLAP-1 as a therapeutic target for periodontal diseases.

  2. 実験的歯周炎モデルマウスにおける好中球誘導性エフェロサイトーシスの検討

    佐藤 理恵, 梶川 哲宏, 野田 武聖, 李 晴玲, 山田 聡

    日本歯周病学会会誌　65　(秋季特別)　128-128　2023/10

    Publisher: (NPO)日本歯周病学会

    ISSN： 0385-0110

    eISSN： 1880-408X

  3. The Dual Roles of Neutrophils in Periodontal Disease: Insights from the Latest Findings on the Regulation of Periodontitis and Disease Progression Peer-reviewed

    Tetsuhiro Kajikawa, Satoru Yamada

    Nihon Shishubyo Gakkai Kaishi (Journal of the Japanese Society of Periodontology)　65　(3)　93-100　2023/09/29

    Publisher: Japanese Society of Periodontology

    DOI： 10.2329/perio.65.93 　

    ISSN： 0385-0110

    eISSN： 1880-408X

  4. Increased STAT3 Activation in Periodontitis Drives Inflammatory Bone Loss Peer-reviewed

    M. Arce, M. Rodriguez-Peña, J. Espinoza-Arrue, R.A. Godoy, M. Reyes, T. Kajikawa, T. Greenwell-Wild, G. Hajishengallis, L. Abusleme, N. Moutsopoulos, N. Dutzan

    Journal of Dental Research　2023/09/12

    Publisher: SAGE Publications

    DOI： 10.1177/00220345231192381 　

    ISSN： 0022-0345

    eISSN： 1544-0591

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    Periodontitis is one of the most prevalent human inflammatory diseases. It is characterized by periodontal tissue destruction, progressively driven by the host response. In this regard, cytokines associated with tissue destruction, such as interleukin (IL)–6 and IL-23, use a common signaling pathway mediated by STAT3. This transcription factor is also needed for IL-17A production, a key mediator in periodontitis pathogenesis. Although several studies have reported increased activation of STAT3 in experimental periodontitis, a detailed characterization of STAT3 activation in human gingival tissues and its involvement in alveolar bone loss has yet to be explored. Using a cross-sectional study design, we detected increased proportions of pSTAT3-positive cells during periodontitis compared with health, particularly in epithelial cells and T cells. Other cell types of hematopoietic and nonhematopoietic origin also display STAT3 activation in gingival tissues. We detected increased STAT3 phosphorylation and expression of STAT3-related genes during experimental periodontitis. Next, we evaluated the role of STAT3 in alveolar bone destruction using a mouse model of STAT3 loss of function (mut- Stat3 mice). Compared with controls, mut- Stat3 mice had reduced alveolar bone loss following ligature-induced periodontitis. We also evaluated pharmacologic inhibition of STAT3 in ligature-induced periodontitis. Like mut- Stat3 mice, mice treated with STAT3 small-molecule inhibitor had reduced bone loss compared with controls. Our results demonstrate that STAT3 activation is increased in epithelial and T cells during periodontitis and indicate a pathogenic role of STAT3 in inflammatory alveolar bone loss.

  5. Prolyl-hydroxylase inhibitor-induced regeneration of alveolar bone and soft tissue in a mouse model of periodontitis through metabolic reprogramming Peer-reviewed

    Elan Zebrowitz, Azamat Aslanukov, Tetsuhiro Kajikawa, Kamila Bedelbaeva, Sam Bollinger, Yong Zhang, David Sarfatti, Jing Cheng, Phillip B. Messersmith, George Hajishengallis, Ellen Heber-Katz

    Frontiers in Dental Medicine　3　2022/11/25

    Publisher: Frontiers Media SA

    DOI： 10.3389/fdmed.2022.992722 　

    eISSN： 2673-4915

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    Bone injuries and fractures reliably heal through a process of regeneration with restoration to original structure and function when the gap between adjacent sides of a fracture site is small. However, when there is significant volumetric loss of bone, bone regeneration usually does not occur. In the present studies, we explore a particular case of volumetric bone loss in a mouse model of human periodontal disease (PD) in which alveolar bone surrounding teeth is permanently lost and not replaced. This model employs the placement of a ligature around the upper second molar for 10 days leading to inflammation and bone breakdown and closely replicates the bacterially-induced inflammatory etiology of human PD to induce bone degeneration. After ligature removal, mice are treated with a timed-release formulation of a small molecule inhibitor of prolylhydroxylases (PHDi; 1,4-DPCA) previously shown to induce epimorphic regeneration of soft tissue in non-regenerating mice. This PHDi induces high expression of HIF-1α and is able to shift the metabolic state from OXPHOS to aerobic glycolysis, an energetic state used by stem cells and embryonic tissue. This regenerative response was completely blocked by siHIF1a. In these studies, we show that timed-release 1,4-DPCA rapidly and completely restores PD-affected bone and soft tissue with normal anatomic fidelity and with increased stem cell markers due to site-specific stem cell migration and/or de-differentiation of local tissue, periodontal ligament (PDL) cell proliferation, and increased vascularization. In-vitro studies using gingival tissue show that 1,4-DPCA indeed induces de-differentiation and the expression of stem cell markers but does not exclude the role of migrating stem cells. Evidence of metabolic reprogramming is seen by the expression of not only HIF-1α, its gene targets, and resultant de-differentiation markers, but also the metabolic genes Glut-1, Gapdh, Pdk1, Pgk1 and Ldh-a in the periodontal tissue.

  6. Complement Is Required for Microbe-Driven Induction of Th17 and Periodontitis. International-journal Peer-reviewed

    Hui Wang, Hidetaka Ideguchi, Tetsuhiro Kajikawa, Dimitrios C Mastellos, John D Lambris, George Hajishengallis

    Journal of immunology (Baltimore, Md. : 1950)　2022/08/26

    DOI： 10.4049/jimmunol.2200338 　

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    In both mice and humans, complement and Th17 cells have been implicated in periodontitis, an oral microbiota-driven inflammatory disease associated with systemic disorders. A recent clinical trial showed that a complement C3 inhibitor (AMY-101) causes sustainable resolution of periodontal inflammation, the main effector of tissue destruction in this oral disease. Although both complement and Th17 are required for periodontitis, it is uncertain how these immune components cooperate in disease development. In this study, we dissected the complement-Th17 relationship in the setting of ligature-induced periodontitis (LIP), a model that previously established that microbial dysbiosis drives Th17 cell expansion and periodontal bone loss. Complement was readily activated in the periodontal tissue of LIP-subjected mice but not when the mice were placed on broad-spectrum antibiotics. Microbiota-induced complement activation generated critical cytokines, IL-6 and IL-23, which are required for Th17 cell expansion. These cytokines as well as Th17 accumulation and IL-17 expression were significantly suppressed in LIP-subjected C3-deficient mice relative to wild-type controls. As IL-23 has been extensively studied in periodontitis, we focused on IL-6 and showed that LIP-induced IL-17 and bone loss required intact IL-6 receptor signaling in the periodontium. LIP-induced IL-6 was predominantly produced by gingival epithelial cells that upregulated C3a receptor upon LIP challenge. Experiments in human gingival epithelial cells showed that C3a upregulated IL-6 production in cooperation with microbial stimuli that upregulated C3a receptor expression in ERK1/2- and JNK-dependent manner. In conclusion, complement links the periodontal microbiota challenge to Th17 cell accumulation and thus integrates complement- and Th17-driven immunopathology in periodontitis.

  7. C3-targeted host-modulation approaches to oral inflammatory conditions Peer-reviewed

    Tetsuhiro Kajikawa, Dimitrios C. Mastellos, Hatice Hasturk, Georgios A. Kotsakis, Despina Yancopoulou, John D. Lambris, George Hajishengallis

    Seminars in Immunology　101608-101608　2022/06

    Publisher: Elsevier BV

    DOI： 10.1016/j.smim.2022.101608 　

    ISSN： 1044-5323

  8. 白血球接着不全症I型関連歯周炎におけるMAIT細胞の同定とその役割

    梶川 哲宏, Hajishengallis George, 山田 聡

    日本歯周病学会会誌　64　(春季特別)　113-113　2022/05

    Publisher: (NPO)日本歯周病学会

    ISSN： 0385-0110

    eISSN： 1880-408X

  9. Developmental endothelial locus-1 protects from hypertension-induced cardiovascular remodeling via immunomodulation. International-journal Peer-reviewed

    Theresa Failer, Michael Amponsah-Offeh, Aleš Neuwirth, Ioannis Kourtzelis, Pallavi Subramanian, Peter Mirtschink, Mirko Peitzsch, Klaus Matschke, Sems M Tugtekin, Tetsuhiro Kajikawa, Xiaofei Li, Anne Steglich, Florian Gembardt, Annika C Wegner, Christian Hugo, George Hajishengallis, Triantafyllos Chavakis, Andreas Deussen, Vladimir Todorov, Irakli Kopaliani

    The Journal of clinical investigation　2022/02/08

    DOI： 10.1172/JCI126155 　

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    The causative role of inflammation in hypertension-related cardiovascular diseases is evident and calls for development of specific immunomodulatory therapies. We tested the therapeutic efficacy and mechanisms of action of developmental endothelial locus-1 (DEL-1), an endogenous anti-inflammatory factor, in angiotensin-II (ANGII)- and DOCA (deoxycorticosterone acetate)-salt-induced cardiovascular organ damage and hypertension. By using mice with endothelial overexpression of DEL-1 (EC-Del1) and performing preventive and interventional studies by injecting recombinant DEL-1 in mice, we showed that DEL-1 improved endothelial function and abrogated aortic adventitial fibrosis, medial thickening and loss of elastin. DEL-1 also protected the mice from cardiac concentric hypertrophy, interstitial and perivascular coronary fibrosis and improved left-ventricular function and myocardial coronary perfusion. DEL-1 prevented aortic stiffness and abolished the progression of hypertension. Mechanistically, DEL-1 acted by inhibiting αvβ3-integrin dependent activation of pro-MMP2 in mice and in human isolated aorta. Moreover, DEL-1 stabilized αvβ3-integrin dependent CD25+FoxP3+ Treg numbers and IL-10 levels, which were associated with decreased pro-inflammatory cell recruitment of inflammatory cells and reduced production of pro-inflammatory cytokines in cardiovascular organs. The demonstrated effects and immune-modulating mechanisms of DEL-1 in abrogation of cardiovascular remodeling and progression of hypertension identify DEL-1 as a potential therapeutic factor.

  10. C3-targeted therapy in periodontal disease: moving closer to the clinic Peer-reviewed

    George Hajishengallis, Hatice Hasturk, John D. Lambris, Danae A. Apatzidou, Georgios N. Belibasakis, Nagihan Bostanci, Patricia M. Corby, Christopher W. Cutler, Francesco D'Aiuto, Evlambia Hajishengallis, Markus Huber-Lang, Effie Ioannidou, Tetsuhiro Kajikawa, Alpdogan Kantarci, Jonathan M. Korostoff, Georgios A. Kotsakis, Tomoki Maekawa, Dimitrios C. Mastellos, Niki M. Moutsopoulos, Srinivas Myneni, Richard Nagelberg, Bo Nilsson, Panos N. Papapanou, Evangelos Papathanasiou, Jan Potempa, Antonio Risitano, S. Esra Sahingur, Atsushi Saito, Anton Sculean, Andreas Stavropoulos, Flavia R. Teles, Maurizio Tonetti, Despina Yancopoulou

    Trends in Immunology　42　(10)　856-864　2021/10

    Publisher: Elsevier {BV}

    DOI： 10.1016/j.it.2021.08.001 　

    ISSN： 1471-4906

  11. Stromal cell-derived DEL-1 inhibits Tfh cell activation and inflammatory arthritis. International-journal Peer-reviewed

    Hui Wang, Xiaofei Li, Tetsuhiro Kajikawa, Jieun Shin, Jong-Hyung Lim, Ioannis Kourtzelis, Kosuke Nagai, Jonathan Korostoff, Sylvia Grossklaus, Ronald Naumann, Triantafyllos Chavakis, George Hajishengallis

    The Journal of clinical investigation　2021/08/17

    DOI： 10.1172/JCI150578 　

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    The secreted protein DEL-1 regulates inflammatory cell recruitment and protects against inflammatory pathologies in animal models. Here, we investigated DEL-1 in inflammatory arthritis using collagen-induced arthritis (CIA) and collagen Ab-induced arthritis (CAIA). In both models, mice with endothelial-specific overexpression of DEL-1 were protected from arthritis relative to WT controls, while arthritis was exacerbated in DEL-1-deficient mice. Compared to WT controls, mice with collagen VI promoter-driven overexpression of DEL-1 in mesenchymal cells were protected against CIA but not CAIA, suggesting a role for DEL-1 in the induction of the arthritogenic Ab response. Indeed, DEL-1 was expressed in perivascular stromal cells of the lymph nodes and inhibited T follicular helper (Tfh) and germinal center B cell responses. Mechanistically, DEL-1 inhibited dendritic cell-dependent induction of Tfh cells by targeting the LFA-1 integrin on T cells. Overall, DEL-1 restrained arthritis through a dual mechanism, one acting locally in the joints and associated with the anti-recruitment function of endothelial cell-derived DEL-1; the other mechanism acting systemically in the lymph nodes and associated with the ability of stromal cell-derived DEL-1 to restrain Tfh responses. DEL-1 may thus be a promising novel therapeutic for the treatment of inflammatory arthritis.

  12. Mouse Model of Loeys–Dietz Syndrome Shows Elevated Susceptibility to Periodontitis via Alterations in Transforming Growth Factor-Beta Signaling International-journal Peer-reviewed

    Satoru Yamada, Kenichiro Tsushima, Masaki Kinoshita, Hiromi Sakashita, Tetsuhiro Kajikawa, Chiharu Fujihara, Hang Yuan, Shigeki Suzuki, Takayuki Morisaki, Shinya Murakami

    Frontiers in Physiology　12　715687-715687　2021/08/11

    Publisher: Frontiers Media SA

    DOI： 10.3389/fphys.2021.715687 　

    eISSN： 1664-042X

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    Loeys–Dietz syndrome (LDS) is a syndromic connective tissue disorder caused by a heterozygous missense mutation in genes that encode transforming growth factor (TGF)-β receptor (<italic>TGFBR</italic>) <italic>1</italic> and <italic>2</italic>. We encountered a patient with LDS, who had severe periodontal tissue destruction indicative of aggressive periodontitis. The patient had a missense mutation in the glycine and serine-rich domain of <italic>TGFBR1</italic> exon 3. This G-to-T mutation at base 563 converted glycine to valine. We established an LDS model knock-in mouse that recapitulated the LDS phenotype. Homozygosity of the mutation caused embryonic lethality and heterozygous knock-in mice showed distorted and ruptured elastic fibers in the aorta at 24 weeks of age and died earlier than wildtype (WT) mice. We stimulated mouse embryonic fibroblasts (MEFs) from the knock-in mouse with TGF-β and examined their responses. The knock-in MEFs showed downregulated <italic>Serpine 1</italic> mRNA expression and phosphorylation of Smad2 to TGF-β compared with WT MEFs. To clarify the influence of TGF-β signaling abnormalities on the pathogenesis or progression of periodontitis, we performed pathomolecular analysis of the knock-in mouse. There were no structural differences in periodontal tissues between WT and LDS model mice at 6 or 24 weeks of age. Micro-computed tomography revealed no significant difference in alveolar bone resorption between WT and knock-in mice at 6 or 24 weeks of age. However, TGF-β-related gene expression was increased significantly in periodontal tissues of the knock-in mouse compared with WT mice. Next, we assessed a mouse periodontitis model in which periodontal bone loss was induced by oral inoculation with the bacterial strain <italic>Porphyromonas gingivalis</italic> W83. After inoculation, we collected alveolar bone and carried out morphometric analysis. <italic>P. gingivalis</italic>-induced alveolar bone loss was significantly greater in LDS model mice than in WT mice. Peritoneal macrophages isolated from <italic>Tgfbr1<italic>G</italic>188V/+</italic> mice showed upregulation of inflammatory cytokine mRNA expression induced by <italic>P. gingivalis</italic> lipopolysaccharide compared with WT macrophages. In this study, we established an LDS mouse model and demonstrated that LDS model mice had elevated susceptibility to <italic>P. gingivalis</italic>-induced periodontitis, probably through TGF-β signal dysfunction. This suggests that TGF-β signaling abnormalities accelerate the pathogenesis or progression of periodontitis.

  13. Mice lacking PLAP-1/asporin counteracts high fat diet-induced metabolic disorder and alveolar bone loss by controlling adipose tissue expansion. International-journal Peer-reviewed

    Hiromi Sakashita, Satoru Yamada, Masaki Kinoshita, Tetsuhiro Kajikawa, Tomoaki Iwayama, Shinya Murakami

    Scientific reports　11　(1)　4970-4970　2021/03/02

    DOI： 10.1038/s41598-021-84512-2 　

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    Adipose tissue fibrosis with chronic inflammation is a hallmark of obesity-related metabolic disorders, and the role of proteoglycans in developing adipose tissue fibrosis is of interest. Periodontal disease is associated with obesity; however, the underlying molecular mechanisms remain unclear. Here we investigated the roles of periodontal ligament associated protein-1 (PLAP-1)/asporin, a proteoglycan preferentially and highly expressed in the periodontal ligament, in obesity-related adipose tissue dysfunction and adipocyte differentiation. It was found that PLAP-1 is also highly expressed in white adipose tissues. Plap-1 knock-out mice counteracted obesity and alveolar bone resorption induced by a high-fat diet. Plap-1 knock-down in 3T3-L1 cells resulted in less lipid accumulation, and recombinant PLAP-1 enhanced lipid accumulation in 3T3-L1 cells. In addition, it was found that primary preadipocytes isolated from Plap-1 knock-out mice showed lesser lipid accumulation than the wild-type (WT) mice. Furthermore, the stromal vascular fraction of Plap-1 knock-out mice showed different extracellular matrix gene expression patterns compared to WT. These findings demonstrate that PLAP-1 enhances adipogenesis and could be a key molecule in understanding the association between periodontal disease and obesity-related metabolic disorders.

  14. The DEL-1/β3 integrin axis promotes regulatory T cell responses during inflammation resolution. International-journal Peer-reviewed

    Xiaofei Li, Alessandra Colamatteo, Lydia Kalafati, Tetsuhiro Kajikawa, Hui Wang, Jong-Hyung Lim, Khalil Bdeir, Kyoung-Jin Chung, Xiang Yu, Clorinda Fusco, Antonio Porcellini, Salvatore De Simone, Giuseppe Matarese, Triantafyllos Chavakis, Veronica De Rosa, George Hajishengallis

    The Journal of clinical investigation　130　(12)　6261-6277　2020/12/01

    DOI： 10.1172/JCI137530 　

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    FOXP3+CD4+ regulatory T cells (Tregs) are critical for immune homeostasis and respond to local tissue cues, which control their stability and function. We explored here whether developmental endothelial locus-1 (DEL-1), which, like Tregs, increases during resolution of inflammation, promotes Treg responses. DEL-1 enhanced Treg numbers and function at barrier sites (oral and lung mucosa). The underlying mechanism was dissected using mice lacking DEL-1 or expressing a point mutant thereof, or mice with T cell-specific deletion of the transcription factor RUNX1, identified by RNA sequencing analysis of the DEL-1-induced Treg transcriptome. Specifically, through interaction with αvβ3 integrin, DEL-1 promoted induction of RUNX1-dependent FOXP3 expression and conferred stability of FOXP3 expression upon Treg restimulation in the absence of exogenous TGF-β1. Consistently, DEL-1 enhanced the demethylation of the Treg-specific demethylated region (TSDR) in the mouse Foxp3 gene and the suppressive function of sorted induced Tregs. Similarly, DEL-1 increased RUNX1 and FOXP3 expression in human conventional T cells, promoting their conversion into induced Tregs with increased TSDR demethylation, enhanced stability, and suppressive activity. We thus uncovered a DEL-1/αvβ3/RUNX1 axis that promotes Treg responses at barrier sites and offers therapeutic options for modulating inflammatory/autoimmune disorders.

  15. An injectable hydrogel-formulated inhibitor of prolyl-4-hydroxylase promotes T regulatory cell recruitment and enhances alveolar bone regeneration during resolution of experimental periodontitis. International-journal Peer-reviewed

    Kosuke Nagai, Hidetaka Ideguchi, Tetsuhiro Kajikawa, Xiaofei Li, Triantafyllos Chavakis, Jing Cheng, Phillip B Messersmith, Ellen Heber-Katz, George Hajishengallis

    FASEB journal : official publication of the Federation of American Societies for Experimental Biology　34　(10)　13726-13740　2020/10

    DOI： 10.1096/fj.202001248R 　

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    The hypoxia-inducible factor 1α (HIF-1α) is critically involved in tissue regeneration. Hence, the pharmacological prevention of HIF-1α degradation by prolyl hydroxylase (PHD) under normoxic conditions is emerging as a promising option in regenerative medicine. Using a mouse model of ligature-induced periodontitis and resolution, we tested the ability of an injectable hydrogel-formulated PHD inhibitor, 1,4-dihydrophenonthrolin-4-one-3-carboxylic acid (1,4-DPCA/hydrogel), to promote regeneration of alveolar bone lost owing to experimental periodontitis. Mice injected subcutaneously with 1,4-DPCA/hydrogel at the onset of periodontitis resolution displayed significantly increased gingival HIF-1α protein levels and bone regeneration, as compared to mice treated with vehicle control. The 1,4-DPCA/hydrogel-induced increase in bone regeneration was associated with elevated expression of osteogenic genes, decreased expression of pro-inflammatory cytokine genes, and increased abundance of FOXP3+ T regulatory (Treg) cells in the periodontal tissue. The enhancing effect of 1,4-DPCA/hydrogel on Treg cell accumulation and bone regeneration was reversed by AMD3100, an antagonist of the chemokine receptor CXCR4 that mediates Treg cell recruitment. In conclusion, the administration of 1,4-DPCA/hydrogel at the onset of periodontitis resolution promotes CXCR4-dependent accumulation of Treg cells and alveolar bone regeneration, suggesting a novel approach for regaining bone lost due to periodontitis.

  16. Frontline Science: Activation of metabolic nuclear receptors restores periodontal tissue homeostasis in mice with leukocyte adhesion deficiency‐1 Peer-reviewed

    Tetsuhiro Kajikawa

    Journal of Leukocyte Biology　108　(5)　1501-1514　2020/05/18

    Publisher: Wiley

    DOI： 10.1002/jlb.5hi0420-648r 　

    ISSN： 0741-5400 1938-3673

    eISSN： 1938-3673

  17. The secreted protein DEL-1 activates a β3 integrin-FAK-ERK1/2-RUNX2 pathway and promotes osteogenic differentiation and bone regeneration. Peer-reviewed

    Yuh DY, Maekawa T, Li X, Kajikawa T, Bdeir K, Chavakis T, Hajishengallis G

    The Journal of biological chemistry　2020/04

    DOI： 10.1074/jbc.ra120.013024 　

  18. Complement C3 as a Target of Host Modulation in Periodontitis Peer-reviewed

    George Hajishengallis, Tetsuhiro Kajikawa, Evlambia Hajishengallis, Tomoki Maekawa, Xiaofei Li, George N. Belibasakis, Nagihan Bostanci, Dimitrios C. Mastellos, Despina Yancopoulou, Hatice Hasturk, John D. Lambris

    Emerging Therapies in Periodontics　13-29　2020

    Publisher: Springer International Publishing

    DOI： 10.1007/978-3-030-42990-4_2 　

  19. Pressure Cycling Technology Assisted Mass Spectrometric Quantification of Gingival Tissue Reveals Proteome Dynamics during the Initiation and Progression of Inflammatory Periodontal Disease. Peer-reviewed

    Bao K, Li X, Kajikawa T, Toshiharu A, Selevsek N, Grossmann J, Hajishengallis G, Bostanci N

    Proteomics　2020/01

    DOI： 10.1002/pmic.201900253 　

  20. Complement-Dependent Mechanisms and Interventions in Periodontal Disease. Peer-reviewed

    Hajishengallis G, Kajikawa T, Hajishengallis E, Maekawa T, Reis ES, Mastellos DC, Yancopoulou D, Hasturk H, Lambris JD

    Frontiers in immunology　2019/03

    DOI： 10.3389/fimmu.2019.00406 　

  21. Macrophage β2-Integrins Regulate IL-22 by ILC3s and Protect from Lethal Citrobacter rodentium-Induced Colitis. Peer-reviewed

    Wang B, Lim JH, Kajikawa T, Li X, Vallance BA, Moutsopoulos NM, Chavakis T, Hajishengallis G

    Cell reports　2019/02

    DOI： 10.1016/j.celrep.2019.01.054 　

  22. DEL-1 promotes macrophage efferocytosis and clearance of inflammation. Peer-reviewed

    Kourtzelis I, Li X, Mitroulis I, Grosser D, Kajikawa T, Wang B, Grzybek M, von Renesse J, Czogalla A, Troullinaki M, Ferreira A, Doreth C, Ruppova K, Chavakis T

    Nature immunology　2018/11

    DOI： 10.1038/s41590-018-0249-1 　

  23. A dysbiotic microbiome triggers TH17 cells to mediate oral mucosal immunopathology in mice and humans. Peer-reviewed

    Dutzan N, Kajikawa T, Abusleme L, Greenwell-Wild T, Zuazo CE, Ikeuchi T, Brenchley L, Abe T, Hurabielle C, Martin D, Morell RJ, Freeman AF, Moutsopoulos NM

    Science translational medicine　2018/10

    DOI： 10.1126/scitranslmed.aat0797 　

  24. Safety profile after prolonged C3 inhibition. Peer-reviewed

    Reis ES, Berger N, Wang X, Koutsogiannaki S, Doot RK, Gumas JT, Foukas PG, Resuello RRG, Tuplano JV, Kukis D, Tarantal AF, Young AJ, Kajikawa T, Lambris JD

    Clinical immunology (Orlando, Fla.)　2018/10

    DOI： 10.1016/j.clim.2018.09.004 　

  25. Fibroblast growth factor-2 inhibits CD40-mediated periodontal inflammation. Peer-reviewed

    Fujihara C, Kanai Y, Masumoto R, Kitagaki J, Matsumoto M, Yamada S, Kajikawa T, Murakami S

    Journal of cellular physiology　234　(5)　7149-7160　2018/10

    DOI： 10.1002/jcp.27469 　

    ISSN： 0021-9541

    eISSN： 1097-4652

  26. The purinergic receptor P2X5 contributes to bone loss in experimental periodontitis. Peer-reviewed

    Kim H, Kajikawa T, Walsh MC, Takegahara N, Jeong YH, Hajishengallis G, Choi Y

    BMB reports　2018/09

    DOI： 10.5483/bmbrep.2018.51.9.126 　

  27. Safety and Efficacy of the Complement Inhibitor AMY-101 in a Natural Model of Periodontitis in Non-human Primates. Peer-reviewed

    Kajikawa T, Briones RA, Resuello RRG, Tuplano JV, Reis ES, Hajishengallis E, Garcia CAG, Yancopoulou D, Lambris JD, Hajishengallis G

    Molecular therapy. Methods & clinical development　2017/08

    DOI： 10.1016/j.omtm.2017.08.001 　

  28. Secreted protein Del-1 regulates myelopoiesis in the hematopoietic stem cell niche. Peer-reviewed

    Mitroulis I, Chen LS, Singh RP, Kourtzelis I, Economopoulou M, Kajikawa T, Troullinaki M, Ziogas A, Ruppova K, Hosur K, Maekawa T, Wang B, Chavakis T

    The Journal of clinical investigation　2017/08

    DOI： 10.1172/jci92571 　

  29. Milk fat globule epidermal growth factor 8 inhibits periodontitis in non-human primates and its gingival crevicular fluid levels can differentiate periodontal health from disease in humans. Peer-reviewed

    Kajikawa T, Meshikhes F, Maekawa T, Hajishengallis E, Hosur KB, Abe T, Moss K, Chavakis T, Hajishengallis G

    Journal of clinical periodontology　2017/04

    DOI： 10.1111/jcpe.12707 　

  30. Transcriptome Reveals Cathepsin K in Periodontal Ligament Differentiation. Peer-reviewed

    Yamada S, Ozaki N, Tsushima K, Yamaba S, Fujihara C, Awata T, Sakashita H, Kajikawa T, Kitagaki J, Yamashita M, Yanagita M, Murakami S

    Journal of dental research　95　(9)　1026-1033　2016/04

    DOI： 10.1177/0022034516645796 　

    ISSN： 0022-0345

    eISSN： 1544-0591

  31. Complement inhibition in pre-clinical models of periodontitis and prospects for clinical application. Peer-reviewed

    Hajishengallis G, Hajishengallis E, Kajikawa T, Wang B, Yancopoulou D, Ricklin D, Lambris JD

    Seminars in immunology　2016/03

    DOI： 10.1016/j.smim.2016.03.006 　

  32. Inhibition of pre-existing natural periodontitis in non-human primates by a locally administered peptide inhibitor of complement C3. Peer-reviewed

    Maekawa T, Briones RA, Resuello RR, Tuplano JV, Hajishengallis E, Kajikawa T, Koutsogiannaki S, Garcia CA, Ricklin D, Lambris JD, Hajishengallis G

    Journal of clinical periodontology　2016/03

    DOI： 10.1111/jcpe.12507 　

  33. PLAP-1/Asporin Regulates TLR2- and TLR4-induced Inflammatory Responses. Peer-reviewed

    Yamaba S, Yamada S, Kajikawa T, Awata T, Sakashita H, Tsushima K, Fujihara C, Yanagita M, Murakami S

    Journal of dental research　94　(12)　1706-1714　2015/09

    Publisher: SAGE Publications

    DOI： 10.1177/0022034515606859 　

    ISSN： 0022-0345

    eISSN： 1544-0591

  34. PLAP-1/Asporin Positively Regulates FGF-2 Activity. Peer-reviewed

    Awata T, Yamada S, Tsushima K, Sakashita H, Yamaba S, Kajikawa T, Yamashita M, Takedachi M, Yanagita M, Kitamura M, Murakami S

    Journal of dental research　94　(10)　1417-1424　2015/08

    Publisher: SAGE Publications

    DOI： 10.1177/0022034515598507 　

    ISSN： 0022-0345

    eISSN： 1544-0591

  35. Characterization of a novel periodontal ligament-specific periostin isoform. Peer-reviewed

    Yamada S, Tauchi T, Awata T, Maeda K, Kajikawa T, Yanagita M, Murakami S

    Journal of dental research　93　(9)　891-897　2014/07

    DOI： 10.1177/0022034514543015 　

    ISSN： 0022-0345

    eISSN： 1544-0591

  36. Inhibitory effects of PLAP-1/asporin on periodontal ligament cells. Peer-reviewed

    Kajikawa T, Yamada S, Tauchi T, Awata T, Yamaba S, Fujihara C, Murakami S

    Journal of dental research　93　(4)　400-405　2014/01

    DOI： 10.1177/0022034513520549 　

    ISSN： 0022-0345

    eISSN： 1544-0591

  37. Iron plays a key role in the cytodifferentiation of human periodontal ligament cells. Peer-reviewed

    Hou J, Yamada S, Kajikawa T, Ozaki N, Awata T, Yamaba S, Fujihara C, Murakami S

    Journal of periodontal research　49　(2)　260-267　2013/05

    DOI： 10.1111/jre.12103 　

    ISSN： 0022-3484

    eISSN： 1600-0765

  38. The Longitudinal Effects of Supportive Periodontal Therapy for the Survival of Teeth in Periodontal Patients

    YAMABA Satoko, MATSUMOTO Wataru, IYAMA Mitsuyoshi, HIGASHIYAMA Yayoi, MATSUI Miki, YAMAGUCHI Taishi, OZAKI Nobuhiro, KOJIMA Yuko, OHARA Hiroyuki, KAJIKAWA Tetsuhiro, OZASA Masao, KITAMURA Masahiro, KASHIWAGI Yoichiro, MIKI Koji, TAUCHI Takushi, TAKEDACHI Masahide, KITAGAKI Jirota, YAMASHITA Motozo, YANAGITA Manabu, NOZAKI Takenori, YAMADA Satoru, SHIMABUKURO Yoshio, MIYAZATO Kousuke, MURAKAMI Shinya, KURIHARA Akiko, SHIMA Miwako, KUBOTA Mikiko, NISHIMURA Makoto, YAMAMOTO Atsushi, YOSHIOKA Eri

    The Japanese Journal of Conservative Dentistry　56　(1)　40-47　2013

    Publisher: The Japanese Society of Conservative Dentistry

    DOI： 10.11471/shikahozon.56.40 　

    ISSN： 0387-2343

    More details Close

    Purpose: The purpose of this study was to evaluate the efficacy of supportive periodontal therapy (SPT) for the tooth survival of periodontitis patients. Methods: Two hundred and sixty-eight periodontal patients who had been maintained for 10 years or more with SPT on an approximately 3-month recall schedule were recruited and their residual teeth and tooth loss were examined. The transition of their residual teeth to tooth loss was compared with that of the Survey of Dental Diseases (2005). Results: At the beginning of SPT, the patients (average age: 50.8) had 24.4 teeth on average. The average tooth loss for 10 years' SPT was 0.22 tooth per patient. The proportion of tooth loss in the periodontitis patients during the SPT was lower than that of the age-comparable subjects in the Survey of Dental Diseases. At the beginning of SPT, 105 patients of our study had fewer residual teeth than the age-comparable subjects in the Survey of Dental Diseases. However, after the SPT (average period: 16.7 years), our patients had more residual teeth than those in the Survey. Conclusion: These results suggest that SPT was effective for the conservation of residual teeth.

  39. Role of ferritin in the cytodifferentiation of periodontal ligament cells. Peer-reviewed

    Hou J, Yamada S, Kajikawa T, Ozaki N, Awata T, Yamaba S, Murakami S

    Biochemical and biophysical research communications　426　(4)　643-648　2012/09

    DOI： 10.1016/j.bbrc.2012.09.008 　

    ISSN： 0006-291X

    eISSN： 1090-2104

  40. Effects of L-ascorbic acid 2-phosphate magnesium salt on the properties of human gingival fibroblasts. Peer-reviewed

    Tsutsumi K, Fujikawa H, Kajikawa T, Takedachi M, Yamamoto T, Murakami S

    Journal of periodontal research　2011/11

    DOI： 10.1111/j.1600-0765.2011.01430.x 　

  41. Suppressive effects of nicotine on the cytodifferentiation of murine periodontal ligament cells. Peer-reviewed

    Yanagita M, Kojima Y, Kawahara T, Kajikawa T, Oohara H, Takedachi M, Yamada S, Murakami S

    Oral diseases　16　(8)　812-817　2010/11

    DOI： 10.1111/j.1601-0825.2010.01693.x 　

    ISSN： 1354-523X

    eISSN： 1601-0825

  42. Periodontal tissue regeneration by implantation of adipose-tissue derived stem cells

    Ozasa Masao, Hashikawa Tomoko, Shimabukuro Yoshio, Iwayama Tomoaki, Hiroyuki Oohara, Kajikawa Tetsuhiro, Anzai Jun, Murakami Shinya

    Program and Abstracts of Annual Meeting of the Japanese Society of Periodontology　2008　66-66　2008

    Publisher: JAPANESE SOCIETY OF PERIODONTOLOGY

    DOI： 10.14833/amjsp.2008s.0.66.0 　

  43. Basic fibroblast growth factor regulates expression of heparan sulfate in human periodontal ligament cells. Peer-reviewed

    Shimabukuro Y, Ichikawa T, Terashima Y, Iwayama T, Oohara H, Kajikawa T, Kobayashi R, Terashima H, Takedachi M, Terakura M, Hashikawa T, Yamada S, Murakami S

    Matrix biology : journal of the International Society for Matrix Biology　27　(3)　232-241　2007/10

    DOI： 10.1016/j.matbio.2007.10.005 　

    ISSN： 0945-053X

Show all ︎Show first 5

Misc. 55

  1. New frontiers in neutrophil research: re-evaluating their roles in periodontal disease and recent insights

    梶川哲宏, 山田聡

    日本歯科医師会雑誌　77　(5)　2024

    ISSN： 0047-1763

  2. マウス歯周病炎モデルを用いた歯周組織MAIT細胞の解析

    野田武聖, 梶川哲宏, 佐藤理恵, LI Qingling, ELFIRA Megasari, 山田聡

    日本歯周病学会会誌(Web)　66　2024

    ISSN： 1880-408X

  3. Oral mucosal immunology, its unique environment with Th17 and neutrophils

    池内友子, 梶川哲宏

    実験医学　41　(9)　2023

    ISSN： 0288-5514

  4. The Dual Roles of Neutrophils in Periodontal Disease: Insights from the Latest Findings on the Regulation of Periodontitis and Disease Progression

    梶川哲宏, 山田聡

    日本歯周病学会会誌(Web)　65　(3)　2023

    ISSN： 1880-408X

  5. 実験的歯周炎モデルマウスにおける好中球誘導性エフェロサイトーシスの検討

    佐藤理恵, 梶川哲宏, 野田武聖, LI Qingling, 山田聡

    日本歯周病学会会誌(Web)　65　2023

    ISSN： 1880-408X

  6. 白血球接着不全症I型関連歯周炎におけるMAIT細胞の同定とその役割

    梶川哲宏, HAJISHENGALLIS George, 山田聡

    日本歯周病学会会誌(Web)　64　2022

    ISSN： 1880-408X

  7. 脂肪分化による脂肪分化調節機構の解明

    阪下 裕美, 山田 聡, 津島 賢一朗, 木下 昌毅, 藤原 千春, 梶川 哲宏, 粟田 敏仁, 山羽 聡子, 村上 伸也

    日本歯周病学会会誌　58　(秋季特別)　114-114　2016/09

    Publisher: (NPO)日本歯周病学会

    ISSN： 0385-0110

    eISSN： 1880-408X

  8. 脂肪分化による脂肪分化調節機構の解明

    阪下裕美, 山田聡, 津島賢一朗, 木下昌毅, 藤原千春, 梶川哲宏, 粟田敏仁, 山羽聡子, 村上伸也

    日本歯周病学会会誌(Web)　58　2016

    ISSN： 1880-408X

  9. 肥満病態形成に対するPLAP-1の関与

    阪下 裕美, 山田 聡, 津島 賢一朗, 梶川 哲宏, 粟田 敏仁, 山羽 聡子, 竹立 匡秀, 村上 伸也

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集　142回　69-69　2015/06

    Publisher: (NPO)日本歯科保存学会

  10. 脂肪細胞分化過程におけるPLAP-1の機能解析

    阪下 裕美, 山田 聡, 津島 賢一朗, 山羽 聡子, 粟田 敏仁, 梶川 哲宏, 竹立 匡秀, 村上 伸也

    日本歯周病学会会誌　57　(春季特別)　111-111　2015/04

    Publisher: (NPO)日本歯周病学会

    ISSN： 0385-0110

    eISSN： 1880-408X

  11. PLAP-1遺伝子多型が歯根膜細胞の機能に与える影響

    梶川 哲宏, 山田 聡, 村上 伸也

    大阪大学歯学雑誌　59　(2)　69-70　2015/04

    Publisher: 大阪大学歯学会

    ISSN： 0473-4629

  12. 脂肪細胞分化過程におけるPLAP-1の機能解析

    阪下裕美, 山田聡, 津島賢一朗, 山羽聡子, 粟田敏仁, 梶川哲宏, 竹立匡秀, 村上伸也

    日本歯周病学会会誌(Web)　57　2015

    ISSN： 1880-408X

  13. TLRを介したPLAP-1の炎症制御機構

    山羽 聡子, 山田 聡, 粟田 敏仁, 阪下 裕美, 津島 賢一朗, 梶川 哲宏, 竹立 匡秀, 柳田 学, 村上 伸也

    日本歯周病学会会誌　56　(春季特別)　102-102　2014/04

    Publisher: (NPO)日本歯周病学会

    ISSN： 0385-0110

    eISSN： 1880-408X

  14. 肥満病態におけるPLAP-1の機能解析

    阪下 裕美, 山田 聡, 梶川 哲宏, 粟田 敏仁, 山羽 聡子, 津島 賢一朗, 竹立 匡秀, 村上 伸也

    日本歯周病学会会誌　56　(春季特別)　109-109　2014/04

    Publisher: (NPO)日本歯周病学会

    ISSN： 0385-0110

    eISSN： 1880-408X

  15. 歯根膜特異的分子PLAP-1によるFGF-2機能の制御

    粟田 敏仁, 山田 聡, 山羽 聡子, 阪下 裕美, 津島 賢一朗, 梶川 哲宏, 北村 正博, 村上 伸也

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集　139回　66-66　2013/10

    Publisher: (NPO)日本歯科保存学会

  16. 歯根膜特異的分子PLAP-1による炎症制御機構解明

    山羽 聡子, 山田 聡, 粟田 敏仁, 阪下 裕美, 津島 賢一朗, 梶川 哲宏, 柳田 学, 北村 正博, 村上 伸也

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集　139回　67-67　2013/10

    Publisher: (NPO)日本歯科保存学会

  17. ヒトPLAP-1発現アデノウイルスの作製

    梶川 哲宏, 山田 聡, 粟田 敏仁, 山羽 聡子, 阪下 裕美, 津島 賢一朗, 村上 伸也

    日本歯周病学会会誌　55　(秋季特別)　112-112　2013/09

    Publisher: (NPO)日本歯周病学会

    ISSN： 0385-0110

    eISSN： 1880-408X

  18. 高齢双生児の歯周病における遺伝因子と環境因子の関与

    三木 康史, 山下 元三, 北垣 次郎太, 池上 久仁子, 久保田 実木子, 粟田 敏仁, 梶川 哲宏, 竹立 匡秀, 柳田 学, 野崎 剛徳, 山田 聡, 久留島 悠子, 松田 謙一, 池邉 一典, 北村 正博, 前田 芳信, 村上 伸也, 大阪ツインリサーチグループ

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集　138回　234-234　2013/05

    Publisher: (NPO)日本歯科保存学会

  19. 低酸素状態が歯根膜細胞のPLAP-1発現に及ぼす影響

    山本 智美, 竹立 匡秀, 伊山 舜吉, 沢田 啓吾, 粟田 敏仁, 山羽 聡子, 梶川 哲宏, 小笹 匡雄, 山田 聡, 村上 伸也

    日本歯周病学会会誌　55　(春季特別)　97-97　2013/04

    Publisher: (NPO)日本歯周病学会

    ISSN： 0385-0110

    eISSN： 1880-408X

  20. PLAP-1ノックアウトマウスの作製と解析

    粟田 敏仁, 山田 聡, 山羽 聡子, 梶川 哲宏, 尾崎 亘弘, 阪下 裕美, 北村 正博, 島袋 善夫, 村上 伸也

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集　137回　68-68　2012/10

    Publisher: (NPO)日本歯科保存学会

  21. PLAP-1 polymorphism in periodontal ligament cell differentiation : Promising avenue for future periodontology

    YAMADA Satoru, KAJIKAWA Tetsuhiro, AWATA Toshihito, YAMABA Satoko, MURAKAMI Shinya

    Nihon Shishubyo Gakkai Kaishi (Journal of the Japanese Society of Periodontology)　54　(3)　252-256　2012/09/03

    Publisher: JAPANESE SOCIETY OF PERIODONTOLOGY

    DOI： 10.2329/perio.54.252 　

    ISSN： 0385-0110

    eISSN： 1880-408X

  22. ヒト歯根膜細胞におけるcathepsin Kの発現局在

    尾崎 亘弘, 山田 聡, 田内 拓史, 梶川 哲宏, 粟田 敏仁, 山羽 聡子, 阪下 裕美, 村上 伸也

    日本歯周病学会会誌　54　(秋季特別)　87-87　2012/09

    Publisher: (NPO)日本歯周病学会

    ISSN： 0385-0110

    eISSN： 1880-408X

  23. 歯根膜細胞の石灰化過程におけるTGF-β誘導性のI型コラーゲン代謝機構

    河原 貴展, 山下 元三, 梶川 哲宏, 前田 憲一郎, 北垣 次郎太, 山田 聡, 北村 正博, 村上 伸也

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集　136回　97-97　2012/05

    Publisher: (NPO)日本歯科保存学会

  24. ヒト歯根膜細胞におけるインフラマソームの発現

    山羽 聡子, 山田 聡, 梶川 哲宏, 尾崎 亘弘, 粟田 敏仁, 柳田 学, 北村 正博, 村上 伸也

    日本歯周病学会会誌　54　(春季特別)　115-115　2012/04

    Publisher: (NPO)日本歯周病学会

    ISSN： 0385-0110

    eISSN： 1880-408X

  25. 歯根膜細胞の石灰化過程におけるTGF-βシグナルの機能解析

    河原 貴展, 山下 元三, 中村 友美, 梶川 哲宏, 前田 憲一郎, 北垣 次郎太, 山田 聡, 北村 正博, 村上 伸也

    日本歯周病学会会誌　54　(春季特別)　143-143　2012/04

    Publisher: (NPO)日本歯周病学会

    ISSN： 0385-0110

    eISSN： 1880-408X

  26. SIRT1による歯根膜細胞の石灰化制御

    中村 友美, 山下 元三, 河原 貴展, 橋本 悠平, 梶川 哲宏, 森 健太, 前田 憲一郎, 北垣 次郎太, 柳田 学, 山田 聡, 北村 正博, 村上 伸也

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集　135回　199-199　2011/09

    Publisher: (NPO)日本歯科保存学会

  27. TLR2/TLR3共刺激が歯肉上皮細胞の免疫応答に及ぼす影響

    森 健太, 柳田 学, 兒嶋 由子, 梶川 哲宏, 中村 友美, 山下 元三, 山田 聡, 北村 正博, 村上 伸也

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集　134回　31-31　2011/05

    Publisher: (NPO)日本歯科保存学会

  28. PLAP-1遺伝子多型の歯根膜恒常性における役割

    梶川 哲宏, 山田 聡, 藤原 千春, 田内 拓史, 尾崎 亘弘, 粟田 敏仁, 山羽 聡子, 村上 伸也

    日本歯周病学会会誌　53　(春季特別)　110-110　2011/04

    Publisher: (NPO)日本歯周病学会

    ISSN： 0385-0110

    eISSN： 1880-408X

  29. ヒト歯根膜細胞におけるCathepsin Kの発現調節

    尾崎 亘弘, 山田 聡, 藤原 千春, 田内 拓史, 梶川 哲宏, 粟田 敏仁, 山羽 聡子, 村上 伸也

    日本歯周病学会会誌　53　(春季特別)　111-111　2011/04

    Publisher: (NPO)日本歯周病学会

    ISSN： 0385-0110

    eISSN： 1880-408X

  30. 歯根膜細胞におけるオートファジーの役割

    中村 友美, 山下 元三, 河原 貴展, 橋本 悠平, 梶川 哲宏, 山田 聡, 北垣 次郎太, 前田 憲一郎, 北村 正博, 村上 伸也

    日本歯周病学会会誌　53　(春季特別)　111-111　2011/04

    Publisher: (NPO)日本歯周病学会

    ISSN： 0385-0110

    eISSN： 1880-408X

  31. 歯根膜細胞においてFGF-2はWnt依存性にBMPシグナルを制御する

    山下元三, 河原貴展, 橋本悠平, 中村友美, 梶川哲弘, 森健太, 前田憲一郎, 北垣次郎太, 柳田学, 山田聡, 野崎剛徳, 北村正博, 村上伸也

    日本歯科保存学会学術大会プログラムおよび講演抄録集(Web)　134th　2011

  32. Regulation of Cathepsin K gene expression in human periodontal ligament cells

    Ozaki Nobuhiro, Yamada Satoru, Fujihara Chiharu, Tauchi Takushi, Kajikawa Tetsuhiro, Awata Toshihito, Yamaba Satoko, Murakami Shinya

    Program and Abstracts of Annual Meeting of the Japanese Society of Periodontology　2011　(0)　37-37　2011

    Publisher: JAPANESE SOCIETY OF PERIODONTOLOGY

    DOI： 10.14833/amjsp.2011s.0.37.0 　

    ISSN： 0385-0110

  33. The role of PLAP-1 polymorphism in periodontal ligament homeostasis

    Kajikawa Tetsuhiro, Yamada Satoru, Fujihara Chiharu, Tauchi Takushi, Ozaki Nobuhiro, Awata Toshihito, Yamaba Satoko, Murakami Shinya

    Program and Abstracts of Annual Meeting of the Japanese Society of Periodontology　2011　(0)　36-36　2011

    Publisher: JAPANESE SOCIETY OF PERIODONTOLOGY

    DOI： 10.14833/amjsp.2011s.0.36.0 　

    ISSN： 0385-0110

  34. The role of autophagy in periodontal ligament cell.

    Nakamura Tomomi, Murakami Shinya, Yamashita Motozo, Kawahara Takanobu, Hashimoto Yuhei, Kajikawa Tetsuhiro, Yamada Satoru, Kitagaki Jirota, Maeda Kenichiro, Kitamura Masahiro

    Program and Abstracts of Annual Meeting of the Japanese Society of Periodontology　2011　(0)　38-38　2011

    Publisher: JAPANESE SOCIETY OF PERIODONTOLOGY

    DOI： 10.14833/amjsp.2011s.0.38.0 　

    ISSN： 0385-0110

  35. ヒト歯根膜組織完全長cDNAライブラリーを用いたCathepsin Kの同定および機能解析

    尾崎 亘弘, 山田 聡, 藤原 千春, 田内 拓史, 梶川 哲宏, 粟田 敏仁, 小澤 康宏, 村上 伸也

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集　133回　35-35　2010/10

    Publisher: (NPO)日本歯科保存学会

  36. 歯根膜細胞においてFGF-2はMAPK依存性にBMPシグナルを抑制する

    河原 貴展, 山下 元三, 橋本 悠平, 梶川 哲宏, 中村 友美, 前田 憲一郎, 山田 聡, 北村 正博, 村上 伸也

    日本歯周病学会会誌　52　(秋季特別)　94-94　2010/09

    Publisher: (NPO)日本歯周病学会

    ISSN： 0385-0110

    eISSN： 1880-408X

  37. FGF-2はMAPK依存性にBMPによるSmad1リン酸化を抑制する

    河原 貴展, 山下 元三, 橋本 悠平, 梶川 哲宏, 前田 憲一郎, 北垣 次郎太, 山田 聡, 北村 正博, 村上 伸也

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集　132回　36-36　2010/05

    Publisher: (NPO)日本歯科保存学会

  38. マウス歯周組織発生過程におけるPLAP-1タンパクの発現解析

    梶川 哲宏, 山田 聡, 小澤 康宏, 藤原 千春, 田内 拓史, 尾崎 亘弘, 村上 伸也

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集　132回　41-41　2010/05

    Publisher: (NPO)日本歯科保存学会

  39. ヒトPLAP-1アスパラギン酸連続配列が歯根膜細胞の石灰化に及ぼす影響について

    梶川 哲宏

    日本歯周病学会会誌　52　(春季特別)　103-103　2010/04

    Publisher: (NPO)日本歯周病学会

    ISSN： 0385-0110

    eISSN： 1880-408X

  40. An aspartic acid repeat polymorphism in human PLAP-1 regulates mineralization of periodontal ligament cells

    Kajikawa Tetsuhiro, Yamada Satoru, Ozawa Yasuhiro, Fujihara Chiharu, Tauchi Takushi, Ozaki Nobuhiro, Murakami Shinya

    Program and Abstracts of Annual Meeting of the Japanese Society of Periodontology　2010　(0)　61-61　2010

    Publisher: JAPANESE SOCIETY OF PERIODONTOLOGY

    DOI： 10.14833/amjsp.2010s.0.61.0 　

  41. Functional analysis of a novel Periostin isoform Type II specific for human periodontal ligament

    Tauchi Takushi, Yamada Satoru, Maeda Kenichiro, Fujihara Chiharu, Kajikawa Tetsuhiro, Ozaki Nobuhiro, Murakami Shinya

    Program and Abstracts of Annual Meeting of the Japanese Society of Periodontology　2010　(0)　62-62　2010

    Publisher: JAPANESE SOCIETY OF PERIODONTOLOGY

    DOI： 10.14833/amjsp.2010s.0.62.0 　

  42. Opposing effects of FGF-2-MAPK on BMP signaling axis in PDLs

    Kawahara Takanobu, Yamashita Motozo, Hashimoto Yuhei, Kajikawa Tetsuhiro, Nakamura Tomomi, Maeda Kenichiro, Yamada Satoru, Kitamura Masahiro, Murakami Shinya

    Program and Abstracts of Annual Meeting of the Japanese Society of Periodontology　2010　(0)　65-65　2010

    Publisher: JAPANESE SOCIETY OF PERIODONTOLOGY

    DOI： 10.14833/amjsp.2010f.0.65.0 　

    ISSN： 0385-0110

  43. TGF-βI型受容体阻害剤による歯根膜細胞の石灰化制御

    河原 貴展, 山下 元三, 梶川 哲宏, 橋本 悠平, 柳田 学, 山田 聡, 北村 正博, 村上 伸也

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集　131回　48-48　2009/10

    Publisher: (NPO)日本歯科保存学会

  44. グルタミン酸シグナルによる歯根膜細胞の分化制御

    藤原 千春, 山田 聡, 田内 拓史, 梶川 哲宏, 尾崎 亘弘, 小澤 康宏, 村上 伸也

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集　131回　64-64　2009/10

    Publisher: (NPO)日本歯科保存学会

  45. マウス歯周組織におけるPLAP-1タンパクの発現

    梶川 哲宏, 山田 聡, 小澤 康宏, 藤原 千春, 田内 拓史, 平野 裕之, 村上 伸也

    日本歯周病学会会誌　51　(春季特別)　104-104　2009/04

    Publisher: (NPO)日本歯周病学会

    ISSN： 0385-0110

    eISSN： 1880-408X

  46. Immunohistochemical Analysis of PLAP-1 in Mouse Periodontal Tissues

    Kajikawa Tetsuhiro, Yamada Satoru, Ozawa Yasuhiro, Fujihara Chiharu, Tauchi Takushi, Hirano Hiroyuki, Murakami Shinya

    Program and Abstracts of Annual Meeting of the Japanese Society of Periodontology　2009　(0)　29-29　2009

    Publisher: JAPANESE SOCIETY OF PERIODONTOLOGY

    DOI： 10.14833/amjsp.2009s.0.29.0 　

  47. 歯根膜特異的Periostinアイソフォームは歯根膜細胞の硬組織形成分化を促進する

    田内 拓史, 山田 聡, 前田 憲一郎, 藤原 千春, 梶川 哲宏, 岩山 智明, 小澤 康宏, 柳田 学, 橋川 智子, 北村 正博, 村上 伸也

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集　129回　17-17　2008/10

    Publisher: (NPO)日本歯科保存学会

  48. 脂肪組織由来未分化間葉系幹細胞の移植による歯周組織再生療法の開発

    小笹 匡雄, 橋川 智子, 島袋 善夫, 岩山 智明, 大原 廣之, 梶川 哲宏, 安齋 純, 村上 伸也

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集　129回　39-39　2008/10

    Publisher: (NPO)日本歯科保存学会

  49. ヒト歯根膜細胞の全遺伝子発現プロファイリング解析により同定されたId1の機能解析

    山田 聡, 米田 晋也, 藤原 千春, 田内 拓史, 梶川 哲宏, 柳田 学, 北村 正博, 村上 伸也

    日本歯周病学会会誌　50　(秋季特別)　106-106　2008/09

    Publisher: (NPO)日本歯周病学会

    ISSN： 0385-0110

    eISSN： 1880-408X

  50. 実験的歯周病モデルを用いた脂肪組織由来間葉系幹細胞の移植による歯周組織再生

    小笹 匡雄, 橋川 智子, 島袋 善夫, 岩山 智明, 大原 廣之, 梶川 哲宏, 安齋 純, 村上 伸也

    日本歯周病学会会誌　50　(春季特別)　151-151　2008/04

    Publisher: (NPO)日本歯周病学会

    ISSN： 0385-0110

    eISSN： 1880-408X

  51. n

    Yamada Satoru, Yoneda Shinya, Fujihara Chiharu, Tauchi Takushi, Kajikawa Tetsuhiro, Yanagita Manabu, Kitamura Masahiro, Murakami Shinya

    Program and Abstracts of Annual Meeting of the Japanese Society of Periodontology　2008　(0)　319-319　2008

    Publisher: JAPANESE SOCIETY OF PERIODONTOLOGY

    DOI： 10.14833/amjsp.2008f.0.319.0 　

    ISSN： 0385-0110

  52. 新規歯根膜特異的Periostinアイソフォームの同定と機能解析

    田内 拓史, 山田 聡, 前田 憲一郎, 小澤 康宏, 米田 晋也, 藤原 千春, 梶川 哲宏, 村上 伸也

    日本歯科保存学雑誌　50　(秋季特別)　45-45　2007/10

    Publisher: (NPO)日本歯科保存学会

    ISSN： 0387-2343

    eISSN： 2188-0808

  53. 抜歯のディシジョンメーキング 抜去歯の臨床評価

    宮里 幸祐, 北村 正博, 栗原 暁子, 森口 善夫, 上山 由希, 木田 賀子, 島 美和子, 中川 典子, 松井 美樹, 岩山 智明, 大原 廣之, 梶川 哲宏, 金本 律子, 川村 聡子, 山口 泰司, 寺島 祥充, 市川 朋生, 島袋 善夫, 村上 伸也

    日本歯科保存学雑誌　50　(秋季特別)　137-137　2007/10

    Publisher: (NPO)日本歯科保存学会

    ISSN： 0387-2343

    eISSN： 2188-0808

  54. メカニカルストレスがヒト歯根膜細胞に及ぼす影響の網羅的遺伝子発現解析

    藤原 千春, 山田 聡, 米田 晋也, 田内 拓史, 梶川 哲宏, 小澤 康宏, 村上 伸也

    日本歯周病学会会誌　49　(秋季特別)　202-202　2007/08

    Publisher: (NPO)日本歯周病学会

    ISSN： 0385-0110

    eISSN： 1880-408X

  55. Gene expression analysis of periodontal ligament cells under mechanical stress

    FUJIHARA CHIHARU, Yamada Satoru, Yoneda Shinya, Tauchi Takushi, Kajikawa Tetsuhiro, Ozawa Yasuhiro, Murakami Shinya

    Program and Abstracts of Annual Meeting of the Japanese Society of Periodontology　2007　(0)　53-53　2007

    Publisher: JAPANESE SOCIETY OF PERIODONTOLOGY

    DOI： 10.14833/amjsp.2007f.0.53.0 　

    ISSN： 0385-0110

Show all ︎Show first 5

Books and Other Publications 2

  1. 特集全身をつなぐ粘膜免疫のエコシステム : 微生物の「共生」と「排除」を両立するしくみを解明し、疾患制御に挑む

    鎌田, 信彦

    羊土社　2023/06

    ISBN: 9784758125680

  2. Emerging Therapies in Periodontics

    2020/06/04

    ISBN: 303042989X

Presentations 12

  1. MAIT Cells Drive Periodontitis Associated With Leukocyte Adhesion Deficiency Type 1

    TETSUHIRO KAJIKAWA

    The 72nd Annual Meeting of Japanese Association for Dental, Oral, and Craniofacial Research　2024/11/16

  2. MAIT 細胞による骨破壊制御 Invited

    梶川哲宏

    第66回歯科基礎医学会学術大会　2024/11/03

  3. The Dual Role of Neutrophils in Periodontal Disease: Protective Immunity and Tissue Destruction Invited

    Tetsuhiro Kajikawa

    2024/10/20

  4. LAD1関連歯周炎におけるMAIT細胞の役割

    梶川哲宏

    第6回 口腔医科学フロンティア研究会　2024/05/18

  5. MAIT Cells Exacerbate Alveolar Bone Loss in Periodontitis Associated with LAD1 Invited

    The 71st Annual Meeting of Japanese Association for Dental Research　2023/11/26

  6. The pivotal role of MAIT cells in periodontitis associated with LAD1 International-presentation Invited

    TETSUHIRO KAJIKAWA

    2023/09/27

  7. The role of mucosal-associated invariant T cells in periodontitis associated with LAD1 Invited

    The role of mucosal-associated invariant T cells in, periodontitis, associated with LAD

    The University of Queensland and Tohoku University Bilateral Dentistry Research Symposium　2023/07/25

  8. 白血球接着不全症I型(LAD-I)関連歯周炎の 発症メカニズムと治療法 Invited

    梶川哲宏

    第48回 日本口腔外科学会北日本支部学術大会　2022/07/10

  9. 白血球接着不全症I型関連歯周炎におけるMAIT細胞の同定とその役割

    梶川哲宏

    第65回春季日本歯周病学会学術大会　2022/06/03

  10. Periodontitis associated with leukocyte adhesion deficiency-I Invited

    Tetsuhiro Kajikawa

    13th Congress of the Colombian Association of Allergy, Asthma and Immunology (ACAAI) and the fifth Meeting of the Colombian Association of Immunology (ACOI)　2021/09/10

  11. The Role of γδT cells in Periodontitis Associated with LAD-I

    Tetsuhiro Kajikawa

    The 5th Penn Periodontal Conference 2021　2021/07/25

  12. Metabolic nuclear receptor signaling and inflammation in periodontitis associated with leukocyte adhesion deficiency Invited

    Tetsuhiro Kajikawa

    Immunobiology Research in Progress　2018/05/11

Show all Show first 5

Research Projects 14

  1. CHEF作製技術を応用した超効率死細胞除去による口腔疾患治療法の革命

    梶川 哲宏, 山田 聡, 大谷 栄毅

    Offer Organization: 日本学術振興会

    System: 科学研究費助成事業

    Category: 挑戦的研究(萌芽)

    Institution: 東北大学

    2024/06/28 - 2026/03/31

  2. シングルセルゲノミクスとPheWAS解析による歯周病の個別化医療・予防の確立

    山田 聡, 鈴木 茂樹, 大槻 晃史, 村上 伸也, 梶川 哲宏

    Offer Organization: 日本学術振興会

    System: 科学研究費助成事業

    Category: 基盤研究(B)

    Institution: 東北大学

    2024/04/01 - 2026/03/31

  3. シングルセルゲノミクスとPheWAS解析による歯周病の個別化医療・予防の確立

    山田 聡, 鈴木 茂樹, 大槻 晃史, 村上 伸也, 梶川 哲宏

    Offer Organization: 日本学術振興会

    System: 科学研究費助成事業

    Category: 基盤研究(B)

    Institution: 東北大学

    2023/04/01 - 2026/03/31

  4. エフェロサイトーシスを基軸とした歯周組織恒常性維持機構の解明と治療への応用

    梶川 哲宏, 鈴木 茂樹, 山田 聡

    Offer Organization: 日本学術振興会

    System: 科学研究費助成事業

    Category: 基盤研究(B)

    Institution: 東北大学

    2024/04/01 - 2025/03/31

  5. 再生指向型エピゲノムに基づく歯周組織再生術前診断法と精密化療法の樹立

    鈴木 茂樹, 根本 英二, 山田 聡, 梶川 哲宏

    Offer Organization: 日本学術振興会

    System: 科学研究費助成事業

    Category: 基盤研究(B)

    Institution: 東北大学

    2024/04/01 - 2025/03/31

  6. 歯周組織特異的CAR-MSC細胞を用いた革新的な歯周組織再生移植治療への挑戦

    山田 聡, 向阪 幸彦, 齋藤 正寛, 梶川 哲宏, 鈴木 茂樹

    Offer Organization: 日本学術振興会

    System: 科学研究費助成事業

    Category: 挑戦的研究(萌芽)

    Institution: 東北大学

    2023/06/30 - 2025/03/31

  7. 再生指向型エピゲノムに基づく歯周組織再生術前診断法と精密化療法の樹立

    鈴木 茂樹, 根本 英二, 山田 聡, 梶川 哲宏

    Offer Organization: 日本学術振興会

    System: 科学研究費助成事業

    Category: 基盤研究(B)

    Institution: 東北大学

    2022/04/01 - 2025/03/31

  8. エフェロサイトーシスを基軸とした歯周組織恒常性維持機構の解明と治療への応用

    梶川 哲宏

    Offer Organization: 日本学術振興会

    System: 科学研究費助成事業 基盤研究(B)

    Category: 基盤研究(B)

    Institution: 東北大学

    2022/04/01 - 2025/03/31

  9. Dysbiotic細菌叢特異的MAIT細胞の開発と歯周炎治療への応用

    梶川 哲宏

    Offer Organization: 日本学術振興会

    System: 科学研究費助成事業 挑戦的研究(萌芽)

    Category: 挑戦的研究(萌芽)

    Institution: 東北大学

    2022/06/30 - 2024/03/31

  10. 疾患由来iPS細胞レジストリとPLAP-1を基軸とした侵襲性歯周炎の分子病態解明

    山田 聡, 森崎 隆幸, 江草 宏, 鈴木 茂樹, 根本 英二, 村上 伸也, 梶川 哲宏

    Offer Organization: 日本学術振興会

    System: 科学研究費助成事業

    Category: 基盤研究(B)

    Institution: 東北大学

    2020/04/01 - 2023/03/31

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    本研究では、未だその発症・進行メカニズムの詳細が不明な侵襲性歯周炎（AgP）において、患者由来iPS細胞レジストリ（AgP-iPS細胞レジストリ）を構築し、同細胞レジストリを用いて網羅的な全ゲノム解析と細胞分化機能解析を同時に行うことで、侵襲性歯周炎の原因となる複数の新たなる遺伝子変異群を決定することを目的としている。さらには、申請者らのこれまでの研究結果から、侵襲性歯周炎原因遺伝子の一つであることが示唆されるPLAP-1/Asporinについて、AgPレジストリにおけるPLAP-1遺伝子多型解析を行うことで、PLAP-1が、侵襲性歯周炎の原因遺伝子であることを証明することを目的としている。2021度は、侵襲性歯周炎患者由来iPS細胞レジストリ構築のため、侵襲性歯周炎患者の歯周基本治療および歯周外科処置時に通常は廃棄される不良肉芽組織を回収し、回収した組織からiPS細胞作製用の培養線維芽細胞を樹立するための学内倫理研究申請を行った。さらには、健常者由来iPS細胞を用いてiPS細胞の培養系ならびに間葉系間質細胞と骨芽細胞分化誘導系の確立を行っている。さらに、侵襲性歯周炎と診断された患者の末梢血からゲノムDNAを抽出し、同DNAを大阪大学侵襲性歯周炎ゲノムバンクへ送ることで、レジストリを構築した。また、PLAP-1遺伝子多型が見られるアスパラギン酸リピート数の差異がPLAP-1タンパクの機能におよぼす影響を解析することを目的として、リピート数の異なる哺乳類細胞由来組み換えPLAP-1タンパクを発現・作製するためのベクターシステムを構築した。

  11. 歯根膜特異的分子PLAP-1遺伝子多型の歯周病疾患感受性への関与

    梶川 哲宏

    Offer Organization: 日本学術振興会

    System: 科学研究費助成事業 若手研究(B)

    Category: 若手研究(B)

    Institution: 大阪大学

    2013/04/01 - 2014/03/31

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    1)in vivo 歯周炎-PLAP-1遺伝子多型解析モデルの構築 a)マウス歯周炎モデルを用いたin vivoにおけるPLAP-1の機能解析 はじめに、C57BL/6 野生型マウスの第二臼歯に対し、Porphyromonas gingivalis(P.g.)を一晩浸漬した絹糸を結紮し、絹糸を結紮した状態で2週間飼育、さらに2週間後に絹糸の除去を行い、絹糸結紮後、2、3、4週間経過した同部位の骨レベルをマイクロCTを用いて解析した。コントロール群として、カルボキシルセルロースを浸漬した絹糸を用いた。その結果、絹糸結紮後、4週間後のマイクロCT解析において、コントロール群と比較し、P.g.群で有意に骨レベルが低いことが明らかとなった。次に、当教室で樹立に成功しているPLAP-1 KOマウスに対し、上記のマウス歯周炎モデルを適応し、野生型マウスと比較・検討した。その結果、P.g.を浸漬した絹糸を用いた際、野生型マウス群と比較し、PLAP-1 KOマウス群において有意に骨レベルが高いことがわかった。これらのマウスの歯肉からmRNAを回収し、リアルタイムPCR法を用いて炎症性サイトカインの発現の検討を行った結果、PLAP-1 KOマウス群においてCXCL10の発現が低いことがわかった。これらのマウスの微細環境で生じている現象について、さらなる詳細な検討が必要である。 b)マウス歯周炎モデルにおけるPLAP-1遺伝子多型と炎症応答の関連の検討 D13型PLAP-1,D14型PLAP-1を発現する5次アデノウイルスの作製を行った。この作製したアデノウイルスを濃縮・精製し、PLAP-1 KOマウス周囲歯肉に感染させることで、PLAP-1遺伝子多型と歯周炎炎症応答の関連を詳細に検討する必要がある。

  12. Gene polymorphism in PLAP-1regulates inflammation of periodontal disease.

    KAJIKAWA Tetsuhiro

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research Grant-in-Aid for Research Activity Start-up

    Category: Grant-in-Aid for Research Activity Start-up

    Institution: Osaka University

    2011 - 2012

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    PLAP-1 inhibited LPS-induced inflammation with mouse periodontal ligament cells(MPDL22). In addition, the D14 allele of PLAP-1 inhibited LPS-induced inflammation more strongly compared to the D13 allele of PLAP-1. However, there was no significant difference of LPS-induced inflammation between PLAP-1 deficient mice and wild type mice. Now, I try to make the mouse model of periodontal disease which can elucidate the correlation between polymorphism in PLAP-1 and periodontal inflammation with D13- and D14-PLAP-1 expressing adenovirus system.

  13. Development of novel minimal intervention methods for periodontal tissue regeneration therapy

    YAMADA Satoru, NOZAKI Takenori, HASHIKAWA Tomoko, KAJIKAWA Tetsuhiro, OZAKI Nobuhiro

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research Grant-in-Aid for Challenging Exploratory Research

    Category: Grant-in-Aid for Challenging Exploratory Research

    Institution: Osaka University

    2010 - 2011

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    In order to develop novel minimal intervention therapies for periodontal tissue regeneration in the future, in this study, we investigated which methods are the most effective for introducing exogenous molecules into mesenchymal tissue stem cells for periodontal tissue regeneration. We found that the electroporation method is the most effective, especially utilizing periodontal ligament stem cells. We could conclude these information might be a first step to developing the future regeneration therapies.

  14. Analysis of novel periodontal ligament-specific molecules identified in human periodontal ligament full-length cDNA database.

    OZAWA Yasuhiro, FUJIHARA Chiharu, KAJIKAWA Tetuhiro, OZAKI Nobuhiro, AWATA Toshihito

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research Grant-in-Aid for Young Scientists (B)

    Category: Grant-in-Aid for Young Scientists (B)

    Institution: Osaka University

    2009 - 2010

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    In this study, I analyzed human periodontal ligament full-length cDNA library ( Full-PerioGen database ) and found several genes which were highly expressed in human periodontal ligament tissues. Among of these genes, I focused on FLJ25143 and Cathepsin K of which functions in periodontal ligament were not known. I found that FLJ25143 and Cathepsin K regulated periodontal ligament cell functions, suggesting involvement of these molecules in homeostasis, repair and regeneration of periodontium.

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Academic Activities 1

  1. The member of the Journal of Clinical Periodontology Editorial Board

    2022/07/01 - Present

    Activity type: Peer review