Updated on 2026/05/19

Information

 

写真a

 
SANO TOMOMI
 
Organization
Faculty of Dental Science Department of Dental Science Assistant Professor
Graduate School of Dental Science Department of Dental Science（Concurrent）
Graduate School of Dental Science Department of Oral Science（Concurrent）
School of Dentistry Department of Dentistry（Concurrent）
Title
Assistant Professor
External link

Degree

  • Ph.D.

Research Interests・Research Keywords

  • Research theme： basic medical science

    Keyword： inflammation, miRNA, singaling

    Research period： 2011.4

Awards

  • 第96回日本薬理学会年会 優秀ポスター賞

    2022.12   日本薬理学会  

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  • 保存学会奨励賞

    2018.6  

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    歯周炎症が、全身性に増幅される機序を脂肪細胞－マクロファージ相互作用の観点から検討する目的で、共培養系を確立し炎症脂肪組織における高発現遺伝子を網羅的に解析した結果、マクロファージと脂肪細胞の共培養系において、成熟樹状細胞を誘引するCCL19の遺伝子発現が亢進することを見出し、CCL19とその受容体CCR7に着目した。遺伝性・食餌性肥満マウスでは、LPS注入後の血清CCL19濃度が増大し、CCR7欠損マウスでは、食餌誘導性肥満およびインスリン抵抗性の発症が抑制され、アディポネクチン経路および熱産生が亢進した。この現象はエピカテキン (EC) を添加した高脂肪食負荷マウスにおいても観察された。また、脂肪組織において炎症細胞浸潤はみられず、CD11c陽性細胞は野生型マウスでのみ観察された。すなわち、CCL19-CCR7経路が成熟樹状細胞の脂肪組織への遊走・浸潤に関与し、アディポネクチンシグナルおよび熱産生機能の抑制を介して肥満、インスリン抵抗性の発症に関与することを世界に先駆けて示したことに新規性がある。

  • 50th Perio Expo 2017 Poster Award

    2017.5   UNC  

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    Epicatechin (EC) intake appears to be beneficial for the prevention of cardiovascular disorders, and it is well known that adipose tissue inflammation is one of the major risk factors for coronary heart diseases. Additionally, periodontal inflammation has been suggested to accelerate cardiovascular risk via enhancing adipose tissue inflammation. The purpose of the present study was to determine the in vitro and in vivo effects of EC on adipose tissue inflammation and obesity.
    DNA microarray analysis was performed to evaluate the effects of EC on gene expression in adipocytes co-cultured with endotoxin-stimulated macrophages. To determine the in vivo effects, C57BL/6 mice were fed either a high-fat diet (HFD) or HFD combined with EC, and metabolic changes were observed.
    EC suppressed the expression of many inflammatory genes in the adipocytes co-cultured with endotoxin-stimulated macrophages. Specifically, EC markedly suppressed chemokine (C-C motif) ligand 19 (CCL19) expression. The in vivo study indicated that mice fed the EC-supplemented HFD were protected from diet-induced obesity and insulin resistance. The expression levels of genes associated with inflammation in adipose tissue and in the liver were downregulated in this group of mice.
    EC exerts beneficial effects for the prevention of adipose tissue inflammation and insulin resistance. Since the mice deficient in the CCL19 receptor were protected from diet-induced obesity and insulin resistance, the beneficial effects of EC could be mediated, at least in part, by marked suppression of CCL19 expression. Thus, EC may also exert beneficial effects against periodontal inflammation-associated augmentation of cardiovascular risk.

Papers

  • miR-6402 targets Bmpr2 and negatively regulates mouse adipogenesis Reviewed

    Malaz Elsheikh, Tomomi Sano, Akiko Mizokami, Yusuke Nakatsu, Tomoichiro Asano, Takashi Kanematsu

    Adipocyte   14 ( 1 )   2025.3

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    Authorship：Corresponding author   Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1080/21623945.2025.2474114

  • Epicatechin suppresses the expression of C-C motif chemokine ligand 19 and ameliorates periodontitis. Reviewed

    Tomomi Sano, Yusuke Nakatsu, Meiqun Yuan, Rongzhi Li, Tomoichiro Asano, Atsushi Yasunaga, Takashi Kanematsu

    Journal of Functional Foods   122   106512   2024.10

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    Authorship：Lead author,　Corresponding author   Language：English   Publishing type：Research paper (scientific journal)  

    マウスモデルを使用し、エピカテキンのC-C motif chemokine ligand 19 (CCL19) を介した歯周炎に対する抑制効果を検討し、エピカテキンの持続的な摂取は歯周炎を軽減することを実証した。

    DOI： 10.1016/j.jff.2024.106512

  • miR-582-5p targets Skp1 and regulates NF-κB signaling-mediated inflammation. Reviewed International journal

    Rongzhi Li, Tomomi Sano, Akiko Mizokami, Takao Fukuda, Takanori Shinjo, Misaki Iwashita, Akiko Yamashita, Terukazu Sanui, Yusuke Nakatsu, Yusuke Sotomaru, Tomoichiro Asano, Takashi Kanematsu, Fusanori Nishimura

    Arch Biochem Biophys   2023.1

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    Authorship：Corresponding author   Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1016/j.abb.2022.109501.

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  • Anti-inflammatory effects of miRNA-146a induced in adipose and periodontal tissues Reviewed

    Taiki Sanada, Tomomi Sano, Yusuke Sotomaru, Rehab Alshargabi, Yosuke Yamawaki, Akiko Yamashita, Hiroaki Matsunaga, Misaki Iwashita, Takanori Shinjo, Takashi Kanematsu, Tomoichiro Asano, Fusanori Nishimura

    Biochemistry and Biophysics Reports   22   2020.7

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    Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)  

    MicroRNA (miRNA) plays an important role in diverse cellular biological processes such as inflammatory response, differentiation and proliferation, and carcinogenesis. miR-146a has been suggested as a negative regulator of the inflammatory reaction. Although, it has been reported as expressed in inflamed adipose and periodontal tissues, however, miR-146a's inhibitory effects against inflammatory response in both the tissues, are not well understood. Therefore, in this study, the inhibitory effects of miR-146a on both adipose and periodontal inflammation, was investigated. In vitro study has revealed that miR-146a transfection into either adipocytes or gingival fibroblasts, has resulted in a reduced cytokine gene expression, observed on co-culturing the cells with macrophages in the presence of lipopolysaccharides (LPS), in comparison to the control miRNA transfected. Similarly, miR-146a transfection into macrophages resulted in a reduced expression of TNF-α gene and protein in response to LPS stimulation. In vivo study revealed that a continuous intravenous miR-146a administration into mice via tail vein, protected the mice from developing high-fat diet-induced obesity and the inflammatory cytokine gene expression was down-regulated in both adipose and periodontal tissues. miR-146a appeared to be induced by macrophage-derived inflammatory signals such as TNF-α by negative feed-back mechanism, and it suppressed inflammatory reaction in both adipose and periodontal tissues. Therefore, miR-146a could be suggested as a potential therapeutic molecule and as a common inflammatory regulator for both obesity-induced diabetes and related periodontal diseases.

    DOI： 10.1016/j.bbrep.2020.100757

  • Ccr7 null mice are protected against diet-induced obesity via Ucp1 upregulation and enhanced energy expenditure. Reviewed International journal

    Sano T, Sanada T, Sotomaru Y, Shinjo T, Iwashita M, Yamashita A, Fukuda T, Sanui T, Asano T, Kanematsu T, Nishimura F

    Nutr Metab   2019.7

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    Authorship：Lead author   Language：Japanese   Publishing type：Research paper (scientific journal)  

    BACKGROUND:
    The chemokine receptor CCR7, expressed on various immune cells, is associated with cell migration and lympho-node homing. Mice lacking Ccr7 are protected from diet-induced obesity and subsequent insulin resistance. We evaluated the mechanism underlying these protective effects from the standpoint of energy expenditure.
    METHODS:
    Wild-type and Ccr7 null mice were fed a high-fat diet, and the regulation of energy metabolism and energy metabolism-related molecules, e.g., Ucp1, Cidea, and Pgc1α, were evaluated.
    RESULTS:
    Food intake did not differ between groups. O2 consumption and CO2 production were higher in Ccr7 null mice than in wild-type mice, despite a similar respiratory quotient and glucose and lipid utilization, suggesting that energy expenditure increased in Ccr7 null mice via enhanced metabolism. In white adipose tissues of Ccr7 null mice, Prdm16, Cd137, Tmem26, Th, and Tbx1 expression increased. Similarly, in brown adipose tissues of Ccr7 null mice, Dio2, Pgc1α, Cidea, Sirt1, and Adiponectin expression increased. In both white and brown adipose tissues, Ucp1 gene and protein expression levels were higher in null mice than in wild-type mice.
    CONCLUSIONS:
    In Ccr7 null mice, browning of white adipocytes as well as the activation of brown adipocytes cause enhanced energy metabolism, resulting in protection against diet-induced obesity.

  • Epicatechin downregulates adipose tissue CCL19 expression and thereby ameliorates diet-induced obesity and insulin resistance. Reviewed International journal

    T Sano, S Nagayasu, S Suzuki, M Iwashita, A Yamashita, T Shinjo, T Sanui, A Kushiyama, T Kanematsu, T Asano, F Nishimura

    Nutr Metab Cardiovasc Dis.   2017.3

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    Authorship：Lead author   Language：Japanese   Publishing type：Research paper (scientific journal)  

    Background and aims Epicatechin (EC) intake has been suggested to be beneficial for the prevention of cardiovascular disorders, and it is well known that adipose tissue inflammation is one of the major risk factors for coronary heart diseases. The purpose of the present study was to determine the in vitro and in vivo effects of EC on adipose tissue inflammation and obesity. Methods and results DNA microarray analysis was performed to evaluate the effects of EC on gene expression in adipocytes co-cultured with bacterial endotoxin-stimulated macrophages. To determine the in vivo effects of the catechin, C57BL/6 mice were fed either a high-fat diet (HFD) or HFD combined with EC, and metabolic changes were observed EC suppressed the expression of many inflammatory genes in the adipocytes co-cultured with endotoxin-stimulated macrophages. Specifically, EC markedly suppressed chemokine (C–C motif) ligand 19 (CCL19) expression. The target cell of EC appeared to macrophages. The in vivo study indicated that mice fed the EC-supplemented HFD were protected from diet-induced obesity and insulin resistance. Accordingly, the expression levels of genes associated with inflammation in adipose tissue and in the liver were downregulated in this group of mice. Conclusions EC exerts beneficial effects for the prevention of adipose tissue inflammation and insulin resistance. Since we previously reported that mice deficient in the CCL19 receptor were protected from diet-induced obesity and insulin resistance, it can be concluded that the beneficial effects of EC could be mediated, at least in part, by marked suppression of CCL19 expression.

  • Protection from diet-induced obesity and insulin resistance in mice lacking CCL19-CCR7 signaling Reviewed International journal

    T sano, M Iwashita, S Nagayasu, A Yamashita, T Shinjo, A Hashikata, T Asano, A Kushiyama, N Ishimaru, Y Takahama, F Nishimura

    Obesity   23 ( 7 )   1460 - 1471   2015.7

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    Authorship：Lead author   Language：Japanese   Publishing type：Research paper (scientific journal)  

    DOI： 10.1002/oby.21127

  • Hyaluronan induces ERK activation with minimal transcriptomic changes in pancreatic α-cells Reviewed

    Suguru Sonoyama, Akiko Mizokami, Tomomi Sano, Eijiro Jimi, Masafumi Moriyama, Takashi Kanematsu

    Biochemistry and Biophysics Reports   45   2026.3

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    Language：English  

  • PRIP/PLCL deficiency activates PI3K–AKT–YAP signaling and promotes organ fibrosis Reviewed

    Meiqun Yuan, Tomomi Sano, Jing Gao, Akiko Mizokami, Takashi Kanematsu

    Cell Communication and Signaling   24 ( 180 )   2026.2

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  • Pin1 mediates metabolic dysfunction-associated steatohepatitis in mice fed high-fat, high-cholesterol diet by regulating both PPARα and acetyl CoA carboxylase Reviewed

    Yusuke Nakatsu, Tomomi Sano, Mikako Nakanishi, Yasuka Matsunaga, Machi Kanna, Takashi Kanematsu, Tomoichiro Asano

    Biochimica et Biophysica Acta - Molecular Basis of Disease   1872 ( 2 )   2026.2

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  • Chronic stress impairs autoinhibition in neurons of the locus coeruleus to increase asparagine endopeptidase activity Reviewed International coauthorship

    Hiroki Toyoda, Doyun Kim, Byeong Geon Koh, Tomomi Sano, Takashi Kanematsu, Seog Bae Oh, Youngnam Kang

    eLife   2025.5

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.7554/eLife.106362.1

  • Role of Testosterone Signaling in Microglia: A Potential Role for Sex-Related Differences in Alzheimer's Disease. Reviewed International coauthorship

    Du H, Mizokami A, Ni J, Zhang S, Yamawaki Y, Sano T, Jimi E, Tanida I, Kanematsu T.

    Adv Sci (Weinh)   e2413375   2025.3

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1002/advs.202413375

  • Lipopolysaccharides from Porphyromonas gingivalis indirectly induce neuronal GSK3beta-dependent synaptic defects and cause cognitive decline in a low-amyloid-beta-concentration environment in Alzheimer's disease. Reviewed International coauthorship

    Gui S, Zeng F, Wu Z, Nonaka S, Sano T, Ni J, Nakanishi H, Moriyama M, Kanematsu T.

    J Alzheimers Dis   13872877251326879   2025.3

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1177/13872877251326879

  • Sex differences in the neuroinflammatory signaling pathway: effect of miRNAs on fatty acid synthesis in microglia. Reviewed International coauthorship

    Zheng H, Mizokami A, Romera-Giner S, Llera-Oyola J, Yamawaki Y, Sano T, Jimi E, García-García F, Kanematsu T.

    Biol Sex Differ.   16 ( 1 )   9   2025.2

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1186/s13293-025-00686-8

  • Prolyl isomerase Pin1 in skeletal muscles contributes to systemic energy metabolism and exercise capacity through regulating SERCA activity Reviewed International journal

    Yusuke Nakatsu, Yasuka Matsunaga, Mikako Nakanishi, Takeshi Yamamotoya, Tomomi Sano, Takashi Kanematsu, Tomoichiro Asano

    Biochemical and Biophysical Research Communications   2024.4

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1016/j.bbrc.2024.150001

  • Prolyl isomerase Pin1 in skeletal muscles contributes to systemic energy metabolism and exercise capacity through regulating SERCA activity Reviewed International journal

    Yusuke Nakatsu, Yasuka Matsunaga, Mikako Nakanishi, Takeshi Yamamotoya, Tomomi Sano, Takashi Kanematsu, Tomoichiro Asano

    Biochemical and Biophysical Research Communications   2024.4

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  • miR-1260b inhibits periodontal bone loss by targeting ATF6β mediated regulation of ER stress Reviewed International journal

    Hayashi C, Fukuda T, Kawakami K, Toyoda M, Nakao Y, Watanabe Y, Shinjo T, Sano T, Iwashita M, Yotsumoto K, Shida M, Taketomi T, Sanui T, Uchiumi T, Kanematsu T, Nishimura F.

    Frontiers in Cell and Developmental Biology   2022.12

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  • miR-1260b inhibits periodontal bone loss by targeting ATF6β mediated regulation of ER stress Reviewed International journal

    Hayashi C, Fukuda T, Kawakami K, Toyoda M, Nakao Y, Watanabe Y, Shinjo T, Sano T, Iwashita M, Yotsumoto K, Shida M, Taketomi T, Sanui T, Uchiumi T, Kanematsu T, Nishimura F.

    Frontiers in Cell and Developmental Biology   2022.12

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  • miR-1260b inhibits periodontal bone loss by targeting ATF6β mediated regulation of ER stress

    Hayashi Chikako, Fukuda Takao, Kawakami Kentaro, Toyoda Masaaki, Nakao Yuki, Watanabe Yukari, Shinjo Takanori, Sano Tomomi, Iwashita Misaki, Yotsumoto Karen, Shida Miyu, Taketomi Takaharu, Sanui Terukazu, Uchiumi Takeshi, Kanematsu Takashi, Nishimura Fusanori

    Frontiers in Cell and Developmental Biology   10   1061216   2022.11   （ ISSN:2296-634X eISSN:2296634X ）

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    Language：English   Publisher：Frontiers Media SA  

    The expression profiles of exosomal microRNAs (miRNAs) are regulated by the microenvironment, and appropriate priming with mesenchymal stem cells (MSCs) is one of the strategies to enhance the paracrine potency of MSCs. Our previous work demonstrated that exosomes from tumor necrosis factor (TNF)-α-primed human gingiva-derived MSCs (GMSCs) could be a therapeutic tool against periodontitis, and that TNFα-inducible exosomal miR-1260b is essential for the inhibition of alveolar bone loss. However, the precise molecular mechanism underlying miR-1260b-mediated inhibition of osteoclastogenesis is not yet fully understood. Here, we found that the activating transcription factor (ATF)-6β, a novel miR-1260b-targeting gene, is critical for the regulation of osteoclastogenesis under endoplasmic reticulum (ER) stress. An experimental periodontal mouse model demonstrated that induction of ER stress was accompanied by enhanced ATF6β expression, and local administration of miR-1260b and ATF6β siRNA using polyethylenimine nanoparticles (PEI-NPs) significantly suppressed the periodontal bone resorption. In periodontal ligament (PDL) cells, the ER stress inducer, tunicamycin, enhanced the expression of the receptor activator of NF-κB ligand (RANKL), while miR-1260b-mediated downregulation of ATF6β caused RANKL inhibition. Furthermore, the secretome from miR-1260b/ATF6β-axis-activated PDL cells inhibited osteoclastogenesis in human CD14^+ peripheral blood-derived monocytes. These results indicate that the miR-1260b/ATF6β axis mediates the regulation of ER stress, which may be used as a novel therapeutic strategy to treat periodontal disease.

    DOI： 10.3389/fcell.2022.1061216

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  • XAF1 overexpression exacerbates diabetes by promoting pancreatic β-cell apoptosis Reviewed International journal

    Yuki Nishimura, Misaki Iwashita, Masato Hayashi, Takanori Shinjo, Yukari Watanabe, Tatsuro Zeze, Akiko Yamashita, Takao Fukuda, Terukazu Sanui, Tomomi Sano, Tomoichiro Asano & Fusanori Nishimura

    Acta Diabetologica   59 ( 10 )   1275 - 1286   2022.7   （ ISSN:0940-5429 eISSN:1432-5233 ）

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    Language：English   Publishing type：Research paper (scientific journal)   Publisher：Springer Science and Business Media LLC  

    Abstract

    Aims

    Pancreatic β-cell apoptosis may be involved in the onset and progression of type 2 diabetes mellitus, although its mechanism remains unclear. We previously demonstrated that macrophage-derived interferon (IFN) β induced X-linked inhibitor of apoptosis–associated factor 1 (XAF1) expression in β-cells and accelerated β-cell apoptosis in vitro. Here, we explored the effects of XAF1 on β-cell function and progression of diabetes in vivo.

    Methods

    Pancreatic β-cell-selective XAF1 overexpressing (Xaf1 Tg) mice were generated. Xaf1 Tg mice and their wild-type (WT) littermates were fed either a normal diet or a 40% or 60% high-fat diet (HFD). The effects of β-cell XAF1 on β-cell apoptosis and exacerbation of diabetes were investigated.

    Results

    Palmitic acid induced IFNβ expression in macrophages, and HFD intake promoted macrophage infiltration in pancreatic islets, both of which cooperatively upregulated XAF1 expression in mouse islets. Furthermore, HFD-fed Xaf1 Tg mice demonstrated increased β-cell apoptosis, lowered insulin expression, and impaired glucose tolerance compared with WT mice fed the same diet. These effects were more pronounced in the 60%HFD group than in the 40%HFD group.

    Conclusions

    Pancreatic β-cell XAF1 expression was enhanced via HFD-induced, macrophage-derived IFNβ, which promoted β-cell apoptosis and led to a reduction in insulin secretion and progression of diabetes. To our knowledge, this is the first report to demonstrate an association between pancreatic β-cell XAF1 overexpression and exacerbation of diabetes, thus providing insight into the mechanism of β-cell mass reduction in diabetes.

    DOI： 10.1007/s00592-022-01930-y

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    Other Link： https://link.springer.com/article/10.1007/s00592-022-01930-y/fulltext.html

  • RANKL elevation activates the NIK/NF-κB pathway, inducing obesity in ovariectomized mice. Reviewed International journal

    Mori K, Mizokami A, Sano T, Mukai S, Hiura F, Ayukawa Y, Koyano K, Kanematsu T, Jimi E.

    J Endocrinol.   254 ( 1 )   27 - 36   2022.5   （ ISSN:0022-0795 eISSN:1479-6805 ）

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    Language：English   Publishing type：Research paper (scientific journal)   Publisher：Journal of Endocrinology  

    Menopausal women are susceptible to visceral obesity, which increases the risk of metabolic disorders. However, the mechanisms of menopause-induced visceral fat accumulation are not fully understood. Circulating levels of receptor activator of nuclear factor-kappa B (NF-κB) ligand (RANKL) are elevated in an animal model of menopause. RANKL, a multifunctional cytokine, activates the NF-κB pathway, which serves as a pivotal mediator of inflammatory responses. Here, we investigated whether RANKL-induced non-canonical NF-κB pathway activation induces inflammation and lipid accumulation in adipose tissues. RANKL induced Tnfa expression via the non-canonical NF-κB pathway in bone marrow cells. We therefore analyzed aly/aly mice, in which the non-canonical NF-κB pathway is not activated, owing to an inactive form of NF-κB-inducing kinase. A postmenopausal obesity model was generated by ovariectomy and subsequent high-fat and high-sucrose diet feeding. In aly/aly mice with postmenopausal obesity, serum RANKL levels were elevated, and hepatic lipid accumulation and adipocyte hypertrophy were suppressed, resulting in reduced macrophage infiltration and inflammatory cytokine mRNA expression in visceral adipose tissue. Furthermore, aly/aly mice showed protection from glucose intolerance and insulin resistance, which were observed in ovariectomized WT obese mice. These findings indicate that non-canonical NF-κB pathway activation via serum RANKL elevation contributes to postmenopausal obesity.

    DOI： 10.1530/JOE-21-0424

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  • A Case Report of Improved Palmoplantar Pustulosis following Periodontal Treatment and Possible Association with Diminished Systemic Subclinical Inflammation Reviewed International journal

    Yamashita A, Sano T, Iwashita M, Nishimura F.

    Case Rep Dermatol Med.   2021.10

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1155/2021/5548760

  • Adipose-specific C-C motif chemokine ligand (CCL) 19 overexpression drives the mice to both insulin resistance and weight gain. Reviewed International journal

    Hayashi M, Iwashita M, Nishimura Y, Shinjo T, Sano T, Yamashita A, Fukuda T, Sanui T, Asano T, Nishimura F.

    BMJ Open Diabetes Res Care.   9 ( 1 )   2021.5

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    DOI： 10.1136/bmjdrc-2020-001871.

  • Expression of PRIP, a phosphatidylinositol 4,5-bisphosphate binding protein, attenuates PI3K/AKT signaling and suppresses tumor growth in a xenograft mouse model Reviewed International journal

    Maetani Y, Asano S, Mizokami A, Yamawaki Y, Sano T, Hirata M, Irifune M, Kanematsu T.

    Biochem Biophys Res Commun.   2021.5

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  • Adipocyte-specific GPRC6A ablation promotes diet-induced obesity by inhibiting lipolysis. Reviewed International journal

    Mukai S, Mizokami A, Otani T, Sano T, Matsuda M, Chishaki S, Gao J, Kawakubo-Yasukochi T, Tang R, Kanematsu T, Takeuchi H, Jimi E, Hirata M.

    J Biol Chem.   2021.1

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  • SPOCK1 induces adipose tissue maturation: New insights into the function of SPOCK1 in metabolism Reviewed International journal

    Rehab Alshargabi, Takanori Shinjo, Misaki Iwashita, Akiko Yamashita, Tomomi Sano, Yuki Nishimura, Masato Hayashi, Tatsuro Zeze, Takao Fukuda, Terukazu Sanui, Fusanori Nishimura

    Biochem Biophys Res Commun   2020.10

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1016/j.bbrc.2020.09.129

  • SPOCK1 Is a Novel Inducer of Epithelial to Mesenchymal Transition in Drug-Induced Gingival Overgrowth. Reviewed International journal

    Alshargabi R, Sano T, Yamashita A, Takano A, Sanada T, Iwashita M, Shinjo T, Fukuda T, Sanui T, Kishida S, Nishimura F.

    Sci Rep.   10 ( 1 )   9785   2020.7

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  • Possible involvement of normalized Pin1 expression level and AMPK activation in the molecular mechanisms underlying renal protective effects of SGLT2 inhibitors in mice. Invited Reviewed International journal

    Inoue MK, Matsunaga Y, Nakatsu Y, Yamamotoya T, Ueda K, Kushiyama A, Sakoda H, Fujishiro M, Ono H, Iwashita M, Sano T, Nishimura F, Morii K, Sasaki K, Masaki T, Asano T

    Diabetol Metab Synd   2019.7

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    Language：Japanese   Publishing type：Research paper (scientific journal)  

  • Prolyl Isomerase Pin1 Suppresses Thermogenic Programs in Adipocytes by Promoting Degradation of Transcriptional Co-activator PRDM16. Reviewed International journal

    Nakatsu Y, Matsunaga Y, Yamamotoya T, Ueda K, Inoue MK, Mizuno Y, Nakanishi M, Sano T, Yamawaki Y, Kushiyama A, Sakoda H, Fujishiro M, Ryo A, Ono H, Minamino T, Takahashi SI, Ohno H, Yoneda M, Takahashi K, Ishihara H, Katagiri H, Nishimura F, Kanematsu T, Yamada T, Asano T.

    Cell Rep.   2019.3

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  • Dental pulp cell-derived powerful inducer of TNF-α comprises PKR containing stress granule rich microvesicles. Reviewed International journal

    Suzuki S, Fukuda T, Nagayasu S, Nakanishi J, Yoshida K, Hirata-Tsuchiya S, Nakao Y, Sano T, Yamashita A, Yamada S, Ohta K, Shiba H, Nishimura F.

    Sci Rep.   2019.3

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  • IL-17A synergistically enhances TNFα-induced IL-6 and CCL20 production in 3T3-L1 adipocytes. Reviewed International journal

    新城 尊徳, 岩下 未咲, 山下 明子, 佐野 朋美, 鶴田　満大, 松永　紘明, 讃井 彰一, 浅野 知一郎, 西村 英紀

    Biochemical and Biophysical Research Communications   477 ( 2 )   241 - 246   2016.8

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  • DPP-IV inhibitor anagliptin exerts anti-inflammatory effects on macrophages, adipocytes, and mouse livers by suppressing NF-kappa B activation Invited Reviewed International journal

    新城 尊徳, 中津祐介, 岩下 未咲, 佐野 朋美, 迫田 秀之, 石原 寿光, 櫛山 暁史, 藤城 緑, 福嶋 俊明, 土谷 佳弘, 鎌田 英明, 西村 英紀, 浅野 知一郎

    AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM   309 ( 3 )   E214 - E223   2015.8

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    Language：Japanese   Publishing type：Research paper (scientific journal)  

    DOI： 10.1152/ajpendo.00553.2014

  • High-fat diet feeding significantly attenuates anagliptin-induced regeneration of islets of Langerhans in streptozotocin-induced diabetic mice Invited Reviewed International journal

    新城 尊徳, 中津 祐介, 岩下 未咲, 佐野 朋美, 迫田 秀之, 石原 寿光, 櫛山 暁史, 藤城 緑, 西村 英紀, 浅野 知一郎

    DIABETOLOGY & METABOLIC SYNDROME   7   2015.6

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    Language：Japanese   Publishing type：Research paper (scientific journal)  

    DOI： 10.1186/s13098-015-0047-y

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Books

  • QUINT DIARY 2023

    佐野朋美他（Role：Joint author）

    クインテッセンス出版株式会社  2023.1 

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    Language：Japanese   Book type：Scholarly book

  • QUINT DIARY 2023

    佐野朋美他（Role：Joint author）

    クインテッセンス出版株式会社  2023.1 

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    Language：Japanese   Book type：Scholarly book

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  • 糖尿病合併症　管理・フォローアップ　Ⅲ章「慢性合併症の管理」．

    佐野朋美、西村英紀（Role：Joint author）

    文光堂  2021.2 

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    Language：Japanese  

  • 月刊糖尿病　6「歯周病と糖尿病」． Vol.11 No.4

    佐野朋美、西村英紀

    2019.10 

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    Language：Japanese  

  • 患者さんのエイジングに備える・高齢者への歯周治療と口腔管理

    佐野 朋美他

    インターアクション株式会社  2018.3 

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    Language：Japanese  

Presentations

  • PLCL-deficient macrophages are associated with poor prognosis in kidney renal clear cell carcinoma

    Tomomi Sano, Akiko Mizokami, Takashi Kanematsu

    第99回日本薬理学会年会  2026.3 

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    Event date： 2026.3

    Language：English  

    Venue：仙台市   Country：Japan  

  • Deficiency of PLCL in Tumor-Associated Macrophages Exacerbates the Tumor Microenvironment and Promotes Cancer Malignancy International conference

    Tomomi Sano, Malaz Elsheikh, Akiko Mizokami, Takashi Kanematsu

    23rd Asian Pacific Congress of Nephology  2025.12  Asian Pacific Society of Nephrology

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    Event date： 2025.12

    Language：English   Presentation type：Poster presentation  

    Venue：Taipei   Country：Taiwan, Province of China  

  • Anti-inflammatory effects of epicatechin in human primary periodontal ligament cells

    Tomomi Sano, Takashi Kanematsu

    第67回歯科基礎医学会学術大会  2025.9  歯科基礎医学会

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    Event date： 2025.9

    Language：English  

    Venue：北九州市  

  • Epicatechin suppresses C-C motif chemokine ligand 19 expression and ameliorates periodontitis International conference

    Tomomi Sano, Meiqun Yuan, Akiko Mizokami, Takashi Kanematsu

    ASCEPT, APFP & APSA Joint Congress  2024.12  Asia Pacific Federation of Pharmacologists

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    Event date： 2024.12

    Language：English   Presentation type：Poster presentation  

    Venue：Malborne   Country：Australia  

  • Epicatechin suppresses C-C motif chemokine ligand 19 expression in gingival fibroblast and ameliorates periodontitis

    Tomomi Sano, Yuan Meiqun, Akiko Mizokami, Takashi Kanematsu

    第66回歯科基礎医学会学術大会  2024.11  歯科基礎医学会

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    Event date： 2024.11

    Language：English  

    Venue：長崎  

  • Deficiency of PLCL in tumor-associated macrophages induces cancer malignancy by exacerbating the tumor microenvironment

    佐野朋美、Malaz Elsheikh、溝上顕子、兼松隆

    第97回日本薬理学会年会  2023.12 

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    Event date： 2023.12

    Language：English  

    Venue：神戸   Country：Japan  

  • Epicatechin exerts anti-inflammatory effect on periodontitis through suppression of CCL19 expression

    Tomomi Sano, Rongzhi Li, Fusanori Nishimura, Takashi Kanematsu

    第96回日本生化学会大会  2023.10 

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    Event date： 2023.10 - 2023.11

    Language：English  

    Venue：福岡   Country：Japan  

  • RAW264.7においてmiR-15b-5pはCcr7を標的とし、M1マクロファージへの分化を抑制する

    佐野朋美、溝上顕子、兼松隆

    第76回日本薬理学会西南部会  2023.10 

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    Event date： 2023.10

    Language：Japanese  

    Venue：沖縄   Country：Japan  

  • Study on the effect of PRIP on the polarization of M1/M2 macrophages

    Tomomi Sano, Malaz Elsheikh, Akiko Mizokami, Tamotsu Kiyoshima, Takashi Kanematsu

    第65回歯科基礎医学会学術大会  2023.9 

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    Event date： 2023.9

    Language：English  

    Venue：東京   Country：Japan  

  • miR-582-5p, that targets Skp1 and suppresses NF-κB signaling-mediated inflammation, is down-regulated in periodontitis and obesity

    Li Rongzhi, Tomomi Sano, Takao Fukuda, Takanori Shinjo, Misaki Iwashita, Akiko Yamashita, Terukazu Sanui, Fusanori Nishimura

    日本歯科保存学会2023年度春季大会 （第158回）  2023.6 

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    Event date： 2023.6

    Language：English  

    Venue：松江   Country：Japan  

  • Regulatory mechanisms of tumor-associated macrophages in the tumor microenvironment

    Tomomi Sano, Du Haiyan, Akiko Mizokami, Takashi Kanematsu

    第64回歯科基礎医学会学術大会  2022.9 

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    Event date： 2023.6

    Language：English  

    Venue：徳島   Country：Japan  

  • Identification and characterization of a microRNA regulating adipocyte inflammation

    Malaz Elsheikh, Tomomi Sano, Akiko Mizokami, Takashi Kanematsu

    第64回歯科基礎医学会学術大会  2022.9 

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    Event date： 2023.6

    Language：English  

    Venue：徳島   Country：Japan  

  • MicroRNA targeting Skp1 regulates inflammatory response through NF-κB signaling pathway 

    Tomomi Sano, Rongzhi Li, Akiko Mizokami, Fusanori Nishimura, Takashi Kanematsu

    第96回日本薬理学会年会  2022.12 

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    Event date： 2023.6

    Language：English  

    Venue：横浜   Country：Japan  

  • Regulatory mechanisms of tumor-associated macrophages in the tumor microenvironment

    Tomomi Sano, Du Haiyan, Akiko Mizokami, Takashi Kanematsu

    第64回歯科基礎医学会学術大会  2022.9 

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    Event date： 2023.6

    Language：English  

    Venue：徳島   Country：Japan  

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  • miR-582-5p, that targets Skp1 and suppresses NF-κB signaling-mediated inflammation, is down-regulated in periodontitis and obesity

    Li Rongzhi, Tomomi Sano, Takao Fukuda, Takanori Shinjo, Misaki Iwashita, Akiko Yamashita, Terukazu Sanui, Fusanori Nishimura

    日本歯科保存学会2023年度春季大会 （第158回）  2023.6 

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    Event date： 2023.6

    Language：English  

    Venue：松江   Country：Japan  

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  • Identification and characterization of a microRNA regulating adipocyte inflammation

    Malaz Elsheikh, Tomomi Sano, Akiko Mizokami, Takashi Kanematsu

    第64回歯科基礎医学会学術大会  2022.9 

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    Event date： 2023.6

    Language：English  

    Venue：徳島   Country：Japan  

    researchmap

  • MicroRNA targeting Skp1 regulates inflammatory response through NF-κB signaling pathway

    Tomomi Sano, Rongzhi Li, Akiko Mizokami, Fusanori Nishimura, Takashi Kanematsu

    第96回日本薬理学会年会  2022.12 

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    Event date： 2023.6

    Language：English  

    Venue：横浜   Country：Japan  

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  • 脂肪組織炎症でCCL19-CCR7経路が制御するmicroRNAの同定

    佐野朋美、Malaz Elsheikh、溝上顕子、兼松隆

    第63回歯科基礎医学会学術大会  2021.10 

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    Event date： 2021.10

    Language：Japanese  

    Venue：Web   Country：Japan  

  • Identification of microRNAs involved in adipose tissue inflammation.

    Tomomi Sano

    2019 Taiwan Academy of Periodontology Annual Meeting and International Symposium  2019.11 

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    Event date： 2019.11

    Language：English  

    Venue：Howard Civil Service International House, Taipei   Country：Taiwan, Province of China  

  • Anti-inflammatory effects of miRNA-146a induced in adipose and periodontal tissues. International conference

    Tomomi Sano

    The 59th General Session of Korean Academy of Periodontology  2019.11 

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    Event date： 2019.11

    Language：English  

    Venue：Gwanggaeto Building, Sejong University, Seoul   Country：Korea, Republic of  

  • 脂肪・歯周組織で発現誘導されるmiRNA-146aによる抗炎症効果の検討

    真田大樹、佐野朋美

    第151回日本歯科保存学会2019年度秋季学術大会  2019.10 

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    Event date： 2019.10

    Language：Japanese  

    Venue：福岡国際会議場（福岡市）   Country：Japan  

  • IDENTIFICATION OF MICRORNAS INVOLVED IN ADIPOSE TISSUE INFLAMMATION. International conference

    Sano Tomomi

    13th Asian Pacific Society of Periodontology Meeting  2019.9 

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    Event date： 2019.9

    Language：English  

    Venue：Royale Chulan, Kuala Lumpur   Country：Malaysia  

  • Increased energy expenditure and resistance to obesity in CCR7KO mice. International conference

    Sano Tomomi

    The 96th General Session of the IADR  2018.7 

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    Event date： 2019.6

    Language：English  

    Country：Japan  

  • The Role of Proteoglycans In Drug Induced Gingival Overgrowth (DIGO)

    Rehab Alshargabi, Tomomi Sano

    第149回日本歯科保存学会2018年度秋季学術大会  2018.11 

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    Event date： 2019.6

    Language：English  

    Country：Japan  

  • 脂肪・歯周組織における抗炎症効果の検討

    眞田大樹、佐野朋美

    平成30年度 日本歯周病学会九州五大学・日本臨床歯周病学会九州支部・合同研修会  2018.11 

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    Event date： 2019.6

    Language：Japanese  

    Country：Japan  

  • 脂肪・歯周組織で発現誘導されるmiRNAによる抗炎症効果の検討

    眞田大樹、佐野朋美

    第62回春季日本歯周病学会学術大会  2019.5 

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    Event date： 2019.5

    Language：Japanese  

    Venue：神奈川県民ホール（横浜市）   Country：Japan  

  • CCR7欠損マウスにおける脂肪および歯周組織炎症抑制機序の考察

    佐野朋美

    第61回秋季日本歯周病学会学術大会  2018.10 

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    Event date： 2018.10

    Language：Japanese  

    Country：Japan  

  • Influences of energy metabolism via CCL19-CCR7 pathway on diet-induced obesity and insulin resistance. International conference

    佐野　朋美

    The 12th meeting of the Asian Pacific Society of Periodontology.  2017.9 

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    Event date： 2018.6

    Language：English  

    Country：Korea, Republic of  

  • Study on the mechanism of increased energy expenditure of CCR7 deficient mouse. International conference

    佐野　朋美

    The 65th Annual Meeting of Japanese Association for Dental Research.  2017.11 

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    Event date： 2018.6

    Language：English  

    Country：Japan  

  • エピカテキンは歯肉線維芽細胞─マクロファージ相互作用による過剰な炎症反応を抑制する

    眞田 大樹、佐野 朋美

    日本歯周病学会60周年記念京都大会  2017.12 

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    Event date： 2018.6

    Language：Japanese  

    Country：Japan  

  • 炎症脂肪/歯周組織における抗炎症分子の探索研究

    眞田 大樹、佐野 朋美

    日本歯科保存学会2018年度春季学術大会  2018.6 

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    Event date： 2018.6

    Language：Japanese  

    Country：Japan  

  • CCR7欠損マウスにおけるエネルギー消費亢進機序についての検討

    佐野　朋美

    日本歯科保存学会2017年度秋季学術大会  2017.10 

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    Event date： 2017.10 - 2018.6

    Language：Japanese  

    Country：Japan  

  • CCL19-CCR7経路を介したエネルギー代謝機構が肥満およびインスリン抵抗性に及ぼす影響の機序に関する検討

    佐野 朋美

    日本歯科保存学会2017年度春季学術大会  2017.6 

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    Event date： 2017.6

    Language：Japanese  

    Venue：青森   Country：Japan  

  • エネルギー代謝機構がCCL19-CCR7経路を介した肥満およびインスリン抵抗性に及ぼす影響に関する検討

    佐野 朋美

    第60回日本糖尿病学会年次学術集会  2017.5 

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    Event date： 2017.5

    Language：Japanese  

    Venue：名古屋   Country：Japan  

  • Epicatechin Down-regulates Adipose Tissue CCL19 Expression, Thereby Ameliorates Diet-induced Obesity and Insulin Resistance International conference

    佐野 朋美

    UNC Perio 2017 EXPO  2017.5 

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    Event date： 2017.5

    Language：English  

    Venue：Chapel Hill, North Carolina   Country：United States  

  • Epicatechin Down-regulates Inflammatory Genes in Adipocytes Co-cultured with Endotoxin-activated Macrophages International conference

    山下 明子, 佐野 朋美

    The 95th General Session & Exhibition of the IADR  2017.3 

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    Event date： 2017.3

    Language：English  

    Venue：San Francisco, Calif.   Country：United States  

  • Epicatechin Down-regulates Adipose Tissue CCL19 Expression, Thereby Ameliorates Diet-induced Obesity International conference

    佐野 朋美

    The 95th General Session & Exhibition of the IADR  2017.3 

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    Event date： 2017.3

    Language：English  

    Venue：San Francisco, Calif.   Country：United States  

  • IL-17Aは3T3-L1脂肪細胞におけるTNF-α誘導性IL-6・CCL20産生を相乗的に増強する

    佐野 朋美

    第145回日本歯科保存学会秋季学術大会  2016.10 

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    Event date： 2017.2

    Language：Japanese  

    Venue：松本   Country：Japan  

  • エピカテキンは脂肪細胞‐マクロファージ相互作用による過剰な炎症反応を抑制する

    佐野 朋美

    第59回秋季日本歯周病学会学術大会  2016.10 

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    Event date： 2017.2

    Language：Japanese  

    Venue：新潟   Country：Japan  

  • TLR-4リガンド刺激マクロファージと共存する脂肪細胞で発現するケモカインの網羅的解析

    佐野 朋美

    第55回春季日本歯周病学会学術大会  2012.5 

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    Event date： 2016.5

    Language：Japanese  

    Venue：札幌コンベンションセンター（北海道）   Country：Japan  

  • CCL19-CCR7経路がエネルギー消費に及ぼす影響に関する検討

    佐野 朋美

    第58回春季日本歯周病学会学術大会  2015.5 

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    Event date： 2015.5

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：幕張メッセ（千葉）   Country：Japan  

  • CCR7経路が肥満およびインスリン抵抗性に及ぼす影響に関する検討

    佐野 朋美

    第57回春季日本歯周病学会学術大会  2014.5 

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    Event date： 2014.5

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：長良川国際会議場（岐阜）   Country：Japan  

  • CCR7経路が肥満およびインスリン抵抗性に及ぼす影響に関する検討

    岩下 未咲, 佐野 朋美

    第57回日本糖尿病学会年次学術集会  2014.5 

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    Event date： 2014.5

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：大阪国際会議場（大阪）   Country：Japan  

  • XAF1の過剰発現は膵β細胞のアポトーシスを促進することで糖尿病を悪化させる

    西村 優輝, 岩下 未咲, 新城 尊徳, 瀬々 起朗, 佐野 朋美, 山下 明子, 西村 英紀

    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  2022.10  (NPO)日本歯科保存学会

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  • アポトーシスシグナル伝達に関与する新規microRNAの同定(Identification of a novel microRNA involving in apoptosis signaling)

    Elsheikh Malaz, Sano Tomomi, Mizokami Akiko, Kanematsu Takashi

    Journal of Oral Biosciences Supplement  2023.9  (一社)歯科基礎医学会

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    Language：English  

  • アルツハイマー病の性差の分子基盤におけるミクログリアの役割解明(Elucidating the role of microglia in the molecular basis of sex differences in Alzheimer's disease)

    Du Haiyan, Mizokami Akiko, Kanematsu Takashi, Sano Tomomi, Yamawaki Yosuke, Jimi Eijiro

    Journal of Oral Biosciences Supplement  2023.9  (一社)歯科基礎医学会

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  • エピカテキンはCCL19の発現抑制を介して歯周病に抗炎症効果を示す

    佐野 朋美, 李 栄智, 西村 英紀, 兼松 隆

    日本生化学会大会プログラム・講演要旨集  2023.10  (公社)日本生化学会

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    Language：Japanese  

  • テストステロンはmiRNA3535を介した脂肪酸合成制御にようりミクログリアにおける炎症反応を抑制する

    鄭 昊林, 溝上 顕子, 兼松 隆, 佐野 朋美, 山脇 洋輔, 自見 英治郎

    日本生化学会大会プログラム・講演要旨集  2023.10  (公社)日本生化学会

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  • テストステロンシグナルはミクログリアにおけるオートファジーを増強する(Testosterone signaling enhances autophagic activity in microglia)

    杜 海妍, 溝上 顕子, 兼松 隆, 佐野 朋美, 山脇 洋輔

    Journal of Oral Biosciences Supplement  2022.9  (一社)歯科基礎医学会

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  • ミクログリアにおけるmiRNA発現の性差(Differences in microRNA expression patterns contribute to sexually differential characteristics of microglia)

    溝上 顕子, 佐野 朋美, 山脇 洋輔, 自見 英治郎, 兼松 隆

    Journal of Oral Biosciences Supplement  2022.9  (一社)歯科基礎医学会

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    Language：Japanese  

  • ミクログリアのオートファジー誘導におけるGPRC6A-テストステロンシグナルの役割

    杜 海妍, 溝上 顕子, 兼松 隆, 佐野 朋美, 山脇 洋輔, 自見 英治郎

    日本生化学会大会プログラム・講演要旨集  2023.10  (公社)日本生化学会

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  • 加齢に伴う病態変化の生化学　リン脂質代謝変調による細胞の癌化機構

    兼松 隆, 浅野 智志, 佐野 朋美, 溝上 顕子, 袁 美群, Malaz Elsheikh

    日本生化学会大会プログラム・講演要旨集  2023.10  (公社)日本生化学会

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    Language：Japanese  

  • 性ホルモンのテストステロンがミクログリアにおけるNF-κB炎症経路を抑制する(Sex hormone testosterone inhibits NF-K B inflammatory pathway in microglia)

    Zheng Haolin, Mizokami Akiko, Kanematsu Takashi, Sano Tomomi, Yamawaki Yosuke, Jimi Eijiro

    Journal of Oral Biosciences Supplement  2023.9  (一社)歯科基礎医学会

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    Language：English  

  • 脂肪組織炎症を制御するmicroRNAの同定(Identification and characterization of a microRNA regulating adipocyte inflammation)

    Elsheikh Malaz, 佐野 朋美, 溝上 顕子, 兼松 隆

    Journal of Oral Biosciences Supplement  2022.9  (一社)歯科基礎医学会

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    Language：English  

  • 腫瘍微小環境における腫瘍随伴マクロファージの制御機構(Regulatory mechanisms of tumor-associated macrophages in the tumor microenvironment)

    佐野 朋美, Du Haiyan, 溝上 顕子, 兼松 隆

    Journal of Oral Biosciences Supplement  2022.9  (一社)歯科基礎医学会

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    Language：Japanese  

  • Skp1を標的としNF-κBシグナルを介した炎症を抑制するmiR-582-5pは歯周炎と肥満において抑制されている(miR-582-5p, that targets Skpl and suppresses NF-κB signaling-mediated inflammation, is down-regulated in periodontitis and obesity)

    Li Rongzhi, Sano Tomomi, Fukuda Takao, Shinjo Takanori, Iwashita Misaki, Yamashita Akiko, Sanui Terukazu, Nishimura Fusanori

    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  2023.5  (NPO)日本歯科保存学会

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  • AKTシグナル伝達の制御分子PRIPは腎線維症の進行を負に制御する(PRIP, a regulatory molecule for AKT signaling, negatively modulates renal fibrosis progression)

    Yuan Meiqun, Sano Tomomi, Mizokami Akiko, Gao Jing, Kanematsu Takashi

    Journal of Oral Biosciences Supplement  2023.9  (一社)歯科基礎医学会

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  • PRIPがM1/M2マクロファージの分極化に与える影響についての検討

    佐野 朋美, Elsheikh Malaz, 溝上 顕子, 清島 保, 兼松 隆

    Journal of Oral Biosciences Supplement  2023.9  (一社)歯科基礎医学会

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    Language：Japanese  

  • Prip欠損によるYAPシグナル経路の活性化は腎維線化を促進する

    袁 美群, 佐野 朋美, 溝上 顕子, 高 靖, 兼松 隆

    日本生化学会大会プログラム・講演要旨集  2023.10  (公社)日本生化学会

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    Language：English  

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MISC

  • Organoid in dentistry: Models for oral biology and disease Invited Reviewed International coauthorship

    Sano, T., Ting-Yi Renn, Kanematsu, T., Ming-Shou Hsieh, Chia-Chen Hsu, Wei-Jen Chang

    Journal of Dental Sciences   2025.5

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    Authorship：Lead author   Language：English  

    DOI： 10.1016/j.jds.2025.05.002

  • Epicatechin: Potential Use as Anti-Obese and Anti-Periodontal Nutrient Invited Reviewed

    Tomomi Sano, Malaz Elsheikh, Takashi Kanematsu

    Current Oral Health Reports   2024.9

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    Authorship：Lead author,　Corresponding author   Language：English   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

    DOI： 10.1007/s40496-024-00390-3

  • The Influence of Periodontal Burden on Metabolic Control of Diabetes - Myth or Reality? - from a Nutritional Perspective.

    西村 英紀, 佐野 朋美, 讃井 彰一

    Current Oral Health Reports   2017.6

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    Language：English   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

Professional Memberships

  • 日本薬理学会

  • The International Association for Dental Research

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  • 日本生化学会

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  • Japanese Association for Oral Biology

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Academic Activities

  • Associate Editor International contribution

    Role(s)： Review, evaluation,　Peer review

    2024 - Present

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    Type：Peer review 

  • 学術論文等の審査 International contribution

    Role(s)： Peer review

    2024

    　More details

    Type：Peer review 

    Number of peer-reviewed articles in foreign language journals：3

  • Screening of academic papers

    Role(s)： Peer review

    2023

    　More details

    Type：Peer review 

    Number of peer-reviewed articles in foreign language journals：2

  • Screening of academic papers

    Role(s)： Peer review

    2022

    　More details

    Type：Peer review 

    Number of peer-reviewed articles in foreign language journals：3

  • Screening of academic papers

    Role(s)： Peer review

    2021

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    Type：Peer review 

    Number of peer-reviewed articles in foreign language journals：2

  • Screening of academic papers

    Role(s)： Peer review

    2020

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    Type：Peer review 

    Number of peer-reviewed articles in foreign language journals：4

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Research Projects

  • UAAT International Young Visiting Scholar Program International coauthorship

    2025.2

    University Academic Alliance in Taiwan  UAAT International Young Visiting Scholar Program  UAAT International Young Visiting Scholar Program

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    Authorship：Principal investigator  Grant type：Joint research

  • Functional analysis of M2 macrophages regulating chronic inflammation in tissue

    Grant number：24K12872  2024 - 2026

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    兼松 隆, 佐野 朋美, 溝上 顕子

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    Authorship：Coinvestigator(s)  Grant type：Scientific research funding

    通常、急性炎症で原因が排除されると炎症は鎮まり組織は修復される。しかし、障害が過大の場合、細胞は遺伝子の発現制御（エピゲノム制御）などを介して、そのダメージを記憶する。ダメージ記憶細胞は、周囲の微小環境に働きかけ、炎症を慢性化させて炎症臓器を線維化という不可逆的な機能不全に陥れる。この病態進行にはマクロファージ（MΦ）の関与が知られるが、詳細なメカニズムは未だ不明である。本研究では、慢性炎症惹起モデルマウスを用いて病態進行におけるMΦの役割について分子レベルで明らかにする。

    CiNii Research

  • miRNAを標的とした薬剤性歯肉増殖症新規治療薬の開発

    Grant number：24K12947  2024 - 2026

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    山下 明子, 佐野 朋美, 西村 英紀

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    Authorship：Coinvestigator(s)  Grant type：Scientific research funding

    薬物性歯肉増殖症(DIGO)は、歯周病を難治性にする。申請者らは、SPOCK1がDIGOの病因に関与すること、SPOCK1過剰発現マウスにサイクロスポリン(CysA)を投与すると、DIGOの病態悪化することを解明した。CysAはカルシニューリン(CN)/NFATシグナルを抑制することで、線維化に関わるコラーゲン発現を亢進させるため、CysA誘導性DIGOの悪化には本経路が関与すると考えられる。本研究では歯肉組織においてNFAT発現抑制時に発現亢進するmiRNAを特定し、そのmiRNA阻害剤の歯肉線維化抑制効果を検証し、DIGOとNFAT抑制による難治性歯周病への治療効果を実証することを目指す。

    CiNii Research

  • マクロファージ機能を制御するmiRNAを応用した新規歯周病治療薬の開発

    Grant number：23K09119  2023 - 2025

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    佐野 朋美

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    Authorship：Principal investigator  Grant type：Scientific research funding

    CCR7は、炎症性マクロファージのマーカー分子であるが、マクロファージによる炎症制御にどのような影響を及ぼすか、またその遺伝子発現の制御機構などについては、未だ明確となっていない。
    そこで本研究では、① 炎症性マクロファージで高発現するCCR7を抑制するmiRNAを特定し、② そのmiRNAに抗炎症効果があることを示し、③ miRNAを内包したカプセルによる歯周病や肥満・インスリン抵抗性改善という治療効果を検証することを目的とする。本研究成果は、歯周炎などの慢性炎症に対する抗炎症作用が期待できる新薬の開発に繋がり、新たな治療法の確立に貢献できる。

    CiNii Research

  • 歯肉増殖症や肥満に関わる新規分子SPOCK1のシグナリング経路の探索

    Grant number：21K09897  2021 - 2023

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    山下 明子, 佐野 朋美, 西村 英紀

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    Authorship：Coinvestigator(s)  Grant type：Scientific research funding

    本研究ではSPOCK1の受容体候補の結合タンパクを探索し、次いでSPOCK1のシグナル伝達経路を検討する。これらの結果を基盤として、SPOCK1過剰発現マウスへ受容体候補分子やシグナリングに関わる分子群の抗体や阻害剤を投与し、歯肉増殖症や肥満の発現への効果を検証することを目指す。本研究成果は、歯肉増殖症のみならず肥満やメタボリックシンドロームの発症に関わるSPOCK1の作用機序を解明するという学術的意義に加えて、歯肉増殖症や肥満の新たな治療標的を見出せる可能性がある。更に将来的には癌の転移の研究や治療法の開発にも繋がる可能性を秘めている。

    CiNii Research

  • Functional analysis of a new anti-cancer molecule that promotes anti-tumor immune responses

    Grant number：21K09817  2021 - 2023

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    兼松 隆, 松田 美穂, 佐野 朋美, 溝上 顕子

    　 More details

    Authorship：Coinvestigator(s)  Grant type：Scientific research funding

    本研究は「がん細胞でPRIPによるPI3K/AKTシグナリング制御が抗腫瘍作用を示す」という我々の研究成果からの研究提案であり、PRIP研究をTAM研究へと展開し腫瘍免疫を制御する新たな機構を明らかにする点に学術的独自性がある。また、頭頸部腫瘍の90% は扁平上皮癌であり、がんの悪性化にEGFR/PI3K/AKTシグナル系が密接に関係することから、ヒト口腔扁平上皮癌と周辺組織TAMのPRIP発現を解析して、口腔癌においてもPRIPを介した抗腫瘍メカニズムを利用した抗がん治療法の開発研究へと研究展開を図る。

    CiNii Research

  • 肥満および歯周炎に共通のmiRNAを標的とした新規抗炎症治療薬の開発

    Grant number：20K18512  2020 - 2022

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Early-Career Scientists

    佐野 朋美

    　 More details

    Authorship：Principal investigator  Grant type：Scientific research funding

    本研究は、脂肪組織において炎症性遺伝子 (mRNA) 発現を制御するmiRNAを特定し、そのmiRNAを封入・保護したカプセルには抗炎症効果があることを検証し、肥満およびインスリン抵抗性、ならびにそれらを合併した歯周病への治療効果を実証することを目的とする。

    CiNii Research

  • SPOCK-1生体タンパクを応用した安全性に優れた革新的歯周病予防薬の開発

    Grant number：19K22721  2019 - 2021

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Challenging Research(Exploratory)

    西村 英紀, 自見 英治郎, 佐野 朋美

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    Authorship：Coinvestigator(s)  Grant type：Scientific research funding

    歯周炎による組織破壊は感染の結果生体で惹起される炎症によってもたらされる。つまり、予防の観点からは、感染源の制御に加え、宿主の破壊因子の制御が効果的である。spock-1は複数のドメインから構成され、cysteine protease阻害ドメインに加え、複数の酵素を阻害する。申請者らは歯肉増殖症モデルとしてSPOCK-1 transgenic (TG) マウスを樹立した。そこで、逆にspock-1は歯周炎等の炎症性組織破壊に対して抑制的に作用するとの仮説を設けた。本申請では、spock-1TGマウスにおいて実験的歯周炎や硬組織の吸収が抑制され、軟組織の治癒が促進されるか否かを検証する。

    CiNii Research

  • 抗炎症miRNA内包エクソソームを用いた肥満糖尿病性歯周炎の新規治療法の開発

    Grant number：18K17071  2018 - 2020

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Early-Career Scientists

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    Authorship：Principal investigator  Grant type：Scientific research funding

  • エピカテキンの抗炎症効果の検証～脂肪組織炎症および実験的歯周炎モデルにおける検討

    Grant number：16H07067  2016 - 2017

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Research Activity start-up

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    Authorship：Principal investigator  Grant type：Scientific research funding

  • CCL19-CCR7経路を標的とした脂肪組織炎症および歯周炎抑制効果の検討

    2016

    平成２８年度 研究活動基礎支援制度 ダイバーシティ研究環境実現イニシアティブ

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    Authorship：Principal investigator  Grant type：On-campus funds, funds, etc.

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Educational Activities

  • 大学院教育
    学部教育

Class subject

  • Aging Science and Pharmacology(Core) D

    2026.12 - 2027.2   Winter quarter

  • 薬理学３

    2026.12 - 2027.2   Winter quarter

  • Aging Science and Pharmacology(Upper-grade) D

    2026.12 - 2027.2   Winter quarter

  • Aging Science and Pharmacology(Core) C

    2026.10 - 2026.12   Fall quarter

  • Aging Science and Pharmacology(Upper-grade) C

    2026.10 - 2026.12   Fall quarter

  • 臨床歯科薬理学

    2026.10 - 2026.12   Fall quarter

  • 薬理学2

    2026.6 - 2026.8   Summer quarter

  • Aging Science and Pharmacology(Core) B

    2026.6 - 2026.8   Summer quarter

  • Aging Science and Pharmacology(Upper-grade) B

    2026.6 - 2026.8   Summer quarter

  • 薬理学１

    2026.4 - 2026.6   Spring quarter

  • Aging Science and Pharmacology(Core) A

    2026.4 - 2026.6   Spring quarter

  • Aging Science and Pharmacology(Upper-grade) A

    2026.4 - 2026.6   Spring quarter

  • 薬理学３

    2025.12 - 2026.2   Winter quarter

  • Aging Science and Pharmacology(Upper-grade) D

    2025.12 - 2026.2   Winter quarter

  • Aging Science and Pharmacology(Core) D

    2025.12 - 2026.2   Winter quarter

  • 臨床歯科薬理学

    2025.10 - 2025.12   Fall quarter

  • Aging Science and Pharmacology(Upper-grade) C

    2025.10 - 2025.12   Fall quarter

  • Aging Science and Pharmacology(Core) C

    2025.10 - 2025.12   Fall quarter

  • リサーチエクスポージャー

    2025.6 - 2026.6   Full year

  • 薬理学2

    2025.6 - 2025.8   Summer quarter

  • Aging Science and Pharmacology(Upper-grade) B

    2025.6 - 2025.8   Summer quarter

  • Aging Science and Pharmacology(Core) B

    2025.6 - 2025.8   Summer quarter

  • 薬理学１

    2025.4 - 2025.6   Spring quarter

  • Aging Science and Pharmacology(Upper-grade) A

    2025.4 - 2025.6   Spring quarter

  • Aging Science and Pharmacology(Core) A

    2025.4 - 2025.6   Spring quarter

  • アーリーエクスポージャー

    2025.4 - 2025.6   Spring quarter

  • 薬理学3

    2024.12 - 2025.2   Winter quarter

  • Aging Science and Pharmacology(Core) D

    2024.12 - 2025.2   Winter quarter

  • Aging Science and Pharmacology(Upper-grade) D

    2024.12 - 2025.2   Winter quarter

  • 臨床歯科薬理学

    2024.10 - 2024.12   Fall quarter

  • Aging Science and Pharmacology(Core) C

    2024.10 - 2024.12   Fall quarter

  • Aging Science and Pharmacology(Upper-grade) C

    2024.10 - 2024.12   Fall quarter

  • Aging Science and Pharmacology(Upper-grade) B

    2024.6 - 2024.8   Summer quarter

  • Aging Science and Pharmacology(Core) B

    2024.6 - 2024.8   Summer quarter

  • 薬理学2

    2024.6 - 2024.8   Summer quarter

  • Aging Science and Pharmacology(Core) A

    2024.4 - 2024.6   Spring quarter

  • Aging Science and Pharmacology(Upper-grade) A

    2024.4 - 2024.6   Spring quarter

  • 薬理学1

    2024.4 - 2024.6   Spring quarter

  • リサーチエクスポージャー

    2024.4 - 2024.6   Spring quarter

  • Aging Science and Pharmacology (Upper-grade) D

    2023.12 - 2024.2   Winter quarter

  • 薬理学3

    2023.12 - 2024.2   Winter quarter

  • Aging Science and Pharmacology(Core) D

    2023.12 - 2024.2   Winter quarter

  • Aging Science and Pharmacology (Upper-grade) C

    2023.10 - 2023.12   Fall quarter

  • 臨床歯科薬理学

    2023.10 - 2023.12   Fall quarter

  • Aging Science and Pharmacology(Core) C

    2023.10 - 2023.12   Fall quarter

  • Aging Science and Pharmacology (Upper-grade) B

    2023.6 - 2023.8   Summer quarter

  • 薬理学2

    2023.6 - 2023.8   Summer quarter

  • Aging Science and Pharmacology(Core) B

    2023.6 - 2023.8   Summer quarter

  • 歯科薬理学

    2023.4 - 2024.3   Full year

  • リサーチエクスポージャー

    2023.4 - 2024.3   Full year

  • 薬理学1

    2023.4 - 2023.6   Spring quarter

  • Aging Science and Pharmacology(Core) A

    2023.4 - 2023.6   Spring quarter

  • Aging Science and Pharmacology (Upper-grade) A

    2023.4 - 2023.6   Spring quarter

  • 歯科薬理学

    2022.4 - 2023.3   Full year

  • 口腔機能分子科学（低年次）

    2022.4 - 2023.3   Full year

  • 口腔機能分子科学（コア）

    2022.4 - 2023.3   Full year

  • リサーチエクスポージャー

    2022.4 - 2022.9   First semester

  • Advanced Dental Science Research（口腔機能分子科学）

    2021.4 - 2022.3   Full year

  • 歯科薬理学

    2021.4 - 2021.9   First semester

  • Advanced Dental Science Research（口腔機能分子科学）

    2020.12 - 2021.2   Winter quarter

  • 歯科薬理学

    2020.10 - 2021.3   Second semester

  • 歯周病学Ⅱ

    2020.4 - 2020.9   First semester

  • 総合歯科学

    2019.10 - 2020.3   Second semester

  • 歯周病学Ⅰ

    2019.10 - 2020.3   Second semester

  • 歯周病学Ⅱ

    2019.4 - 2019.9   First semester

  • 総合歯科学

    2018.10 - 2019.3   Second semester

  • 歯周病学Ⅱ

    2018.4 - 2018.9   First semester

  • 歯周病学Ⅰ

    2017.10 - 2018.3   Second semester

  • 総合歯科学

    2017.10 - 2018.3   Second semester

  • 総合歯科学

    2016.10 - 2017.3   Second semester

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FD Participation

  • 2025.6   Role：Participation   Title：ＷＨＯ口腔保健プログラムでの仕事：ユニバーサルヘルスカバレッジ達成に向けて

    Organizer：[Undergraduate school/graduate school/graduate faculty]

  • 2020.6   Role：Participation   Title：ジャーナルをめぐる現状と論文の投稿・入手について

    Organizer：[Undergraduate school/graduate school/graduate faculty]

  • 2019.6   Role：Participation   Title：科研費申請のススメ

    Organizer：[Undergraduate school/graduate school/graduate faculty]

  • 2018.10   Role：Panelist   Title：馬出地区3部局合同男女共同参画FD

    Organizer：[Undergraduate school/graduate school/graduate faculty]

  • 2018.8   Role：Participation   Title：IR室による歯学研究院の研究力分析

    Organizer：[Undergraduate school/graduate school/graduate faculty]

  • 2018.3   Role：Participation   Title：東京医歯大における国家試験対策の実践

    Organizer：[Undergraduate school/graduate school/graduate faculty]

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Teaching Student Awards

  • 歯科基礎医学会モリタ優秀発表賞

    Year and month of award：2024.11

    Classification of award-winning students：Doctoral student   Name of award-winning student：Malaz Elsheikh

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    優秀発表

Outline of Social Contribution and International Cooperation activities

  • UAAT International Young Visiting Scholar Program

Travel Abroad

  • 2025.2 - 2025.3

    Staying countory name 1：Taiwan, Province of China   Staying institution name 1：Taipei Medical University

Year of medical license acquisition

  • 2011