九州大学 研究者情報
論文一覧
新城 尊徳(しんじよう たかのり) データ更新日:2021.06.02

助教 /  歯学研究院 歯学部門 口腔機能修復学講座


原著論文
1. Nakao Y, Fukuda T, Zhang Q, Sanui T, Shinjo T, Kou X, Chen C, Liu D, Watanabe Y, Hayashi C, Yamato H, Yotsumoto K, Tanaka U, Taketomi T, Uchiumi T, Le AD, Shi S, Nishimura F., Exosomes from TNF-α-treated human gingiva-derived MSCs enhance M2 macrophage polarization and inhibit periodontal bone loss, Acta Biomater, 10.1016/j.actbio.2020.12.046., 2021.03.
2. 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., Biochemical and biophysical research communications, 10.1016/j.bbrc.2020.09.129, 2020.10, SPOCK1 is a calcium-binding matricellular proteoglycan that has been extensively studied in several cancer cells. Previously, we generated a mouse line overexpressing SPOCK1 (Spock1-Tg mouse) and showed that SPOCK1 might play an important role in drug-induced gingival overgrowth, indicating that it possesses physiological functions in non-cancer diseases as well. Although SPOCK1 was reported to be secreted from human adipocytes, its role in adipocyte physiology has not been addressed yet. In this study, SPOCK1 protein expression was confirmed in pancreas, adipose tissues, spleen, and liver of normal diet (ND)-fed mice. Interestingly, SPOCK1 was up-regulated in the pancreas and adipose tissues of the high-fat diet (HFD)-fed mice. Spock1-Tg mice fed with ND showed increased maturation in epididymal and inguinal adipose tissues. In addition, Spock1 overexpression strongly decreased expression of UCP-1 in adipose tissues, suggesting that SPOCK1 might regulate thermogenic function through suppression of UCP-1 expression. Finally, exogenous SPOCK1 treatment directly accelerated the differentiation of 3T3-L1 adipocytes, accompanied by the up-regulation of adipocyte differentiation-related gene expression. In conclusion, we demonstrated for the first time that SPOCK1 induced adipocyte differentiation via the up-regulation of adipogenesis-related genes..
3. 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, 100757-100757, 2020.07, 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..
4. Rehab Alshargabi, Tomomi Sano, Akiko Yamashita, Aiko Takano, Taiki Sanada, Misaki Iwashita, Takanori Shinjo, Takao Fukuda, Terukazu Sanui, Shosei Kishida, Fusanori Nishimura, SPOCK1 is a novel inducer of epithelial to mesenchymal transition in drug-induced gingival overgrowth, Scientific reports , 2020.07.
5. Karen Yotsumoto, Terukazu Sanui, Urara Tanaka, Hiroaki Yamato, Rehab Alshargabi, Takanori Shinjo, Yuki Nakao, Yukari Watanabe, Chikako Hayashi, Takaharu Taketomi, Takao Fukuda, Fusanori Nishimura , Amelogenin Downregulates Interferon Gamma-Induced Major Histocompatibility Complex Class II Expression Through Suppression of Euchromatin Formation in the Class II Transactivator Promoter IV Region in Macrophages, Frontiers in Immunol, 10.3389/fimmu.2020.00709, 11, 709, 2020.05.
6. Sano T., Nagayasu S., Suzuki S., Iwashita M., Yamashita A., Shinjo T., Sanui T., Kushiyama A., Kanematsu T., Asano T., Nishimura F., Epicatechin downregulated adipose tissue CCL19 expression and thereby ameliorates diet-induced obesity and insulin resistance., Nutr Metab Cardiovasc Dis, 10.1016/j.numecd.2016.11.008, 37, 30, 249-259, 2019.07.
7. Takano A., Fukuda T., Shinjo T., Iwashita M., Matsuzaki E., Yamamichi K., Takeshita M., Sanui T., Nishimura F, Angiopoietin-like protein 2 is a positive regulator of osteoblast differentiation., Metabolism, 10.1016/j.metabol.2017.01.006., 69, 157-260, 2019.07.
8. Gordin D, Shah H, Shinjo T, St-Louis R, Qi W, Park K, Paniagua SM, Pober DM, Wu IH, Bahnam V, Brissett MJ, Tinsley LJ, Dreyfuss JM, Pan H, Dong Y, Niewczas MA, Amenta P, Sadowski T, Kannt A, Keenan HA, King GL., Characterization of Glycolytic Enzymes and Pyruvate Kinase M2 in Type 1 and 2 Diabetic Nephropathy., Diabetes Care, 10.2337/dc18-2585. , 42, 7, 1263-1273, 2019.07.
9. Shinjo T, Ishikado A, Hasturk H, Pober DM, Paniagua SM, Shah H, Wu IH, Tinsley LJ, Matsumoto M, Keenan HA, Van Dyke TE, Genco RJ, King GL., Characterization of periodontitis in people with type 1 diabetes of 50 years or longer duration., J Periodontol., 10.1002/JPER.18-0735., 90, 6, 565-575, 2019.06.
10. Tsuruta M., Iwashita M., Shinjo T., Matsunaga H., Yamashita A., Nishimura F., Metabolic endotoxemia-activated macrophages promote pancreatic β cell death via IFNβ-Xaf1 pathway., Horm Metab Res, 10.1055/s-0043-121467, 50, 2, 160-167, 2018.02.
11. Matsunaga H, Iwashita M, Shinjo T, Yamashita A, Tsuruta M, Nagasaka S, Taniguchi A, Fukushima M, Watanabe N, Nishimura F., Adipose tissue complement factor B promotes adipocyte maturation., Biochem Biophys Res Commun, 10.1016/j.bbrc.2017.11.069., 495, 1, 740-748, 2018.01.
12. Park K, Li Q, Evcimen ND, Rask-Madsen C, Maeda Y, Maddaloni E, Yokomizo H, Shinjo T, St-Louis R, Fu J, Gordin D, Khamaisi M, Pober D, Keenan H, King GL., Exogenous Insulin Infusion Can Decrease Atherosclerosis in Diabetic Rodents by Improving Lipids, Inflammation, and Endothelial Function., Arterioscler Thromb Vasc Biol. , 10.1161/ATVBAHA.117.310291., 38, 1, 92-101, 2018.01.
13. Sano T, Iwashita M, Nagayasu S, Yamashita A, Shinjo T, Hashikata A, Asano T, Kushiyama A, Ishimaru N, Takahama Y, Nishimura F., Protection from diet-induced obesity and insulin resistance in mice lacking CCL-19–CCR7 signaling., Obesity, 10.1002/oby.21127., 23, 7, 1460-1471, 2015.06.
14. Okubo H, Nakatsu Y, Sakoda H, Kushiyama A, Fujishiro M, Fukushima T, Matsunaga Y, Ohno H, Yoneda M, Kamata H, Shinjo T, Iwashita M, Nishimura F, Asano T., Interactive roles of gut microbiota and gastrointestinal motility in the development of inflammatory disorders., Inflammation and Cell Signaling, 10.14800/ics.643, 2, 1, 2015.05.
15. Okubo H, Nakatsu Y, Kushiyama A, Fujishiro M, Fukushima T, Matsunaga Y, Ohno H, Yoneda M, Kamata H, Shinjo T, Iwashita M, Nishimura F, Asano T., Mosapride citrate improves nonalcoholic steatohepatitis with increased fecal lactic acid bacteria and plasma glucagon-like peptide-1 level in a rodent model., American Journal of Physiology Gastrointestinal Liver and Physiology, 10.1152/ajpgi.00198.2014, 308, 2, G151-G158, 2015.04.
16. Hashikata A, Yamashita A, Suzuki S, Nagayasu S, Shinjo T, Taniguchi A, Fukushima M, Nakai Y, Nin K, Watanabe N, Asano T, Abiko Y, Kushiyama A, Nagasaka S, Nishimura F., The inflammation-lipocalin2 axis may contribute to the development of chronic kidney disease., Nephrology Dialysis Transplantation, 10.1093/ndt/gft449, 29, 3, 611-618, 2014.05.
17. Iwashita M, Nakatsu Y, Sakoda H, Fujishiro M, Kushiyama A, Fukushima T, Kumamoto S, Shinjo T, Kamata H, Nishimura F, Asano T., Valsartan restores inflammatory response by macrophages in adipose and hepatic tissues of LPS-infused mice., Adipocyte, 2, 1, 28-32, 2013.01.
18. Shinjo T, Zhang J, Nakatsu Y, Guo Y, Sakoda H, Yamamotoya T, Otani Y, Okubo H, Kushiyama A, Fujishiro M, Fukushima T, Tsuchiya Y, Kamata H, Iwashita M, Nishimura F,Katagiri H, Takahashi S, Kurihara H, Ushida T, Asano T., Par14 protein associates with insulin receptor substrate 1(IRS-1), thereby enhancing insulin-induced IRS-1 phosphorylation and metabolic actions., Journal of Biological Chemistry, 10.1074/jbc.M113.485730, 288, 28, 20692-20701, 2013.07.
19. Shinjo T, Nakatsu Y, Iwashita M, Sano T, Sakoda H, Ishihara H, Kushiyama A, Fujishiro M, Fukushima T, Tsuchiya Y, Kamata H, Nishimura F, Asano T., DPP-4 inhibitor anagliptin exerts anti-inflammatory effects on macrophages, adipocytes, and mouse livers by suppressing NF-κB activation., American Journal of Physiolosy Endocrinology and Metabolism, 10.1152/ajpendo.00553.2014, 309, 3, E214-E223, 2015.05.
20. Shinjo T, Nakatsu Y, Iwashita M, Sano T, Sakoda H, Ishihara H, Kushiyama A, Fujishiro M, Nishimura F, Asano T., High-fat diet feeding significantly attenuates anagliptin-induced regeneration of islets of Langerhans in streptozotocin-induced diabetic mice., Diabetology and Metabic Syndrome, 10.1186/s13098-015-0047-y, 7, 50, 2015.06.
21. Shinjo T., Iwashita M., Yamashita A., Sano T., Matsugana H., Tsuruta M., Sanui T., Asano T., Nishimura F, IL-17A synergistically enhances TNFα-induced IL-6 and CCL20 production in 3T3-L1 adipocytes., Biochem and Biophys Res Commun, 10.1016/j.bbrc.2016.06.049., 477, 2, 241-246, 2016.08.

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