| 佐野 朋美（さの ともみ） | データ更新日：2024.04.25 |
助教 ／
歯学研究院
歯学部門
| 1. | Yusuke Nakatsu, Yasuka Matsunaga, Mikako Nakanishi, Takeshi Yamamotoya, Tomomi Sano, Takashi Kanematsu, Tomoichiro Asano, Prolyl isomerase Pin1 in skeletal muscles contributes to systemic energy metabolism and exercise capacity through regulating SERCA activity, Biochemical and Biophysical Research Communications, 150001, 2024.04. |
| 2. | Li R, Sano T, Mizokami A, Fukuda T, Shinjo T, Iwashita M, Yamashita A, Sanui T, Nakatsu Y, Sotomaru Y, Asano T, Kanematsu T, Nishimura F, miR-582-5p targets Skp1 and regulates NF-κB signaling-mediated inflammation., Arch Biochem Biophys, 10.1016/j.abb.2022.109501., 2023.01. |
| 3. | 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., miR-1260b inhibits periodontal bone loss by targeting ATF6β mediated regulation of ER stress, Frontiers in Cell and Developmental Biology, 2022.12. |
| 4. | Yuki Nishimura, Misaki Iwashita, Masato Hayashi, Takanori Shinjo, Yukari Watanabe, Tatsuro Zeze, Akiko Yamashita, Takao Fukuda, Terukazu Sanui, Tomomi Sano, Tomoichiro Asano & Fusanori Nishimura , XAF1 overexpression exacerbates diabetes by promoting pancreatic β-cell apoptosis, Acta Diabetologica, 10.1007/s00592-022-01930-y, 2022.07. |
| 5. | Mori K, Mizokami A, Sano T, Mukai S, Hiura F, Ayukawa Y, Koyano K, Kanematsu T, Jimi E., RANKL elevation activates the NIK/NF-κB pathway, inducing obesity in ovariectomized mice., J Endocrinol., 10.1530/JOE-21-0424, 254, 1, 27-36, 2022.05. |
| 6. | Yamashita A, Sano T, Iwashita M, Nishimura F., A Case Report of Improved Palmoplantar Pustulosis following Periodontal Treatment and Possible Association with Diminished Systemic Subclinical Inflammation, Case Rep Dermatol Med., 10.1155/2021/5548760, 2021.10. |
| 7. | Hayashi M, Iwashita M, Nishimura Y, Shinjo T, Sano T, Yamashita A, Fukuda T, Sanui T, Asano T, Nishimura F., Adipose-specific C-C motif chemokine ligand (CCL) 19 overexpression drives the mice to both insulin resistance and weight gain., BMJ Open Diabetes Res Care., 10.1136/bmjdrc-2020-001871., 9, 1, e001871, 2021.05. |
| 8. | Maetani Y, Asano S, Mizokami A, Yamawaki Y, Sano T, Hirata M, Irifune M, Kanematsu T., Expression of PRIP, a phosphatidylinositol 4,5-bisphosphate binding protein, attenuates PI3K/AKT signaling and suppresses tumor growth in a xenograft mouse model, Biochem Biophys Res Commun. , 2021.05. |
| 9. | 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., Adipocyte-specific GPRC6A ablation promotes diet-induced obesity by inhibiting lipolysis., J Biol Chem., 2021.01. |
| 10. | Rehab Alshargabi, Takanori Shinjo, Misaki Iwashita, Akiko Yamashita, Tomomi Sano, Yuki Nishimura, Masato Hayashi, Tatsuro Zeze, Takao Fukuda, Terukazu Sanui, Fusanori Nishimura, SPOCK1 induces adipose tissue maturation: New insights into the function of SPOCK1 in metabolism, Biochem Biophys Res Commun, 10.1016/j.bbrc.2020.09.129, doi: 10.1016/j.bbrc.2020.09.129, 2020.10. |
| 11. | Alshargabi R, Sano T, Yamashita A, Takano A, Sanada T, Iwashita M, Shinjo T, Fukuda T, Sanui T, Kishida S, Nishimura F., SPOCK1 Is a Novel Inducer of Epithelial to Mesenchymal Transition in Drug-Induced Gingival Overgrowth., Sci Rep., 10, 1, 9785, 2020.07. |
| 12. | Taiki Sanada, Tomomi Sano, Yusuke Sotomaru, Rehab Alshargabi, Yosuke Yamawaki, Akiko Yamashita, Hiroaki Matsunaga, Misaki Iwashita, Takanori Shinjo, Takashi Kanematsu, Tomoichiro Asano, Fusanori Nishimura, Anti-inflammatory effects of miRNA-146a induced in adipose and periodontal tissues, Biochemistry and Biophysics Reports, 10.1016/j.bbrep.2020.100757, 22, 2020.07, [URL], 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.. |
| 13. | 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, Possible involvement of normalized Pin1 expression level and AMPK activation in the molecular mechanisms underlying renal protective effects of SGLT2 inhibitors in mice., Diabetol Metab Synd, 2019.07. |
| 14. | Sano T, Sanada T, Sotomaru Y, Shinjo T, Iwashita M, Yamashita A, Fukuda T, Sanui T, Asano T, Kanematsu T, Nishimura F, Ccr7 null mice are protected against diet-induced obesity via Ucp1 upregulation and enhanced energy expenditure., Nutr Metab, 2019.07, 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.. |
| 15. | 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., Dental pulp cell-derived powerful inducer of TNF-α comprises PKR containing stress granule rich microvesicles., Sci Rep., 2019.03. |
| 16. | 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., Prolyl Isomerase Pin1 Suppresses Thermogenic Programs in Adipocytes by Promoting Degradation of Transcriptional Co-activator PRDM16., Cell Rep., 2019.03. |
| 17. | T Sano, S Nagayasu, S Suzuki, M Iwashita, A Yamashita, T Shinjo, T Sanui, A Kushiyama, T Kanematsu, T Asano, F Nishimura, Epicatechin downregulates adipose tissue CCL19 expression and thereby ameliorates diet-induced obesity and insulin resistance., Nutr Metab Cardiovasc Dis., 2017.03, 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.. |
| 18. | 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, IL-17A synergistically enhances TNFα-induced IL-6 and CCL20 production in 3T3-L1 adipocytes., Biochemical and Biophysical Research Communications, 477, 2, 241-246, 2016.08. |
| 19. | 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, DPP-IV inhibitor anagliptin exerts anti-inflammatory effects on macrophages, adipocytes, and mouse livers by suppressing NF-kappa B activation, AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM, 10.1152/ajpendo.00553.2014, 309, 3, E214-E223, 2015.08. |
| 20. | T sano, M Iwashita, S Nagayasu, A Yamashita, T Shinjo, A Hashikata, T Asano, A Kushiyama, N Ishimaru, Y Takahama, F Nishimura, Protection from diet-induced obesity and insulin resistance in mice lacking CCL19-CCR7 signaling, Obesity, 10.1002/oby.21127, 23, 7, 1460-1471, 2015.07. |
| 21. | 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, High-fat diet feeding significantly attenuates anagliptin-induced regeneration of islets of Langerhans in streptozotocin-induced diabetic mice, DIABETOLOGY & METABOLIC SYNDROME, 10.1186/s13098-015-0047-y, 7, 2015.06. |
本データベースの内容を無断転載することを禁止します。