『徳島大学 教育・研究者情報データベース (EDB)』---[学外] /
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登録内容 (EID=327751)

EID=327751EID:327751, Map:0, LastModified:2018年1月6日(土) 17:05:49, Operator:[廣島 佑香], Avail:TRUE, Censor:0, Owner:[廣島 佑香], Read:継承, Write:継承, Delete:継承.
種別 (必須): 学術論文 (審査論文) [継承]
言語 (必須): 英語 [継承]
招待 (推奨):
審査 (推奨): Peer Review [継承]
カテゴリ (推奨): 研究 [継承]
共著種別 (推奨): 国際共著 (徳島大学内研究者と国外研究機関所属研究者との共同研究) [継承]
学究種別 (推奨):
組織 (推奨):
著者 (必須): 1.廣島 佑香 ([徳島大学.大学院医歯薬学研究部.歯学域.口腔科学部門.基礎歯学系.口腔微生物学])
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2.坂本 英次郎 ([徳島大学.病院.診療科.歯科.歯周病科(第二保存科)])
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3.吉田 賀弥 ([徳島大学.大学院医歯薬学研究部.歯学域.口腔科学部門.口腔保健学系.口腔保健教育学]/[徳島大学.歯学部.口腔保健学科.口腔保健基礎学講座])
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4.阿部 佳織
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5.成石 浩司 ([徳島大学.病院.診療科.歯科.歯周病科(第二保存科)])
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6.山本 武範
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7.篠原 康雄 ([徳島大学.先端酵素学研究所.基幹研究部門])
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8.木戸 淳一 ([徳島大学.大学院医歯薬学研究部.歯学域.口腔科学部門.臨床歯学系.歯周歯内治療学])
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9. (英) Geczy L Carolyn (日) (読)
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題名 (必須): (英) Advanced glycation end-products and Porphyromonas gingivalis lipopolysaccharide increase calprotectin expression in human gingival epithelial cells.  (日)    [継承]
副題 (任意):
要約 (任意): (英)   (日) Accumulation of advanced glycation end-products (AGEs) in periodontal tissues of patients with diabetes mellitus aggravates periodontitis, but the mechanisms are unknown. Calprotectin, a heterocomplex of S100A8 and S100A9 proteins, is a constitutive cytoplasmic component of healthy gingival epithelial cells. This study aimed at investigating the effects of AGE and Porphyromonas gingivalis lipopolysaccharide (PgLPS) on calprotectin expression in the human gingival epithelial cell line OBA-9. AGE and PgLPS increased the expression of S100A8 and S100A9 mRNAs, and AGE + PgLPS co-stimulation amplified their expression in OBA-9 cells. A higher concentration of calprotectin in cell lysates was also induced by stimulation with AGE and/or PgLPS. S100A8 was mainly translocated from the nucleus to the cytoplasm by AGE stimulation, while cytoplasmic localization of S100A9 was not altered following stimulation with AGE and/or PgLPS. Calprotectin was found in the cytoplasm of BSA-treated cells, but cytoplasmic and nuclear localization was observed following stimulation with AGE and/or PgLPS. AGE-induced S100A8, and S100A9 mRNA expression was partially suppressed by RAGE-specific siRNA. In contrast, PgLPS-induced S100A8 and S100A9 mRNA expression was strongly suppressed by TLR2-specific siRNA. Furthermore, the inhibition of p38, JNK MAPK, and NF-κB attenuated AGE- and PgLPS-induced S100A8 and S100A9 mRNA expression. Taken together, these results demonstrate that AGE acts in synergy with PgLPS to stimulate RAGE and TLR2 expression and activate p38, JNK MAPK, and NF-κB signaling pathways, resulting in increased activation of calprotectin (S100A8/S100A9) in human gingival epithelial cells. Our results suggest that calprotectin may be involved in the pathogenesis of diabetic periodontitis. This article is protected by copyright. All rights reserved.   [継承]
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誌名 (必須): Journal of Cellular Biochemistry ([Wiley-Liss, Inc.])
(pISSN: 0730-2312, eISSN: 1097-4644)

ISSN (任意): 1097-4644
ISSN: 0730-2312 (pISSN: 0730-2312, eISSN: 1097-4644)
Title: Journal of cellular biochemistry
Title(ISO): J Cell Biochem
Publisher: Wiley
 (NLM Catalog  (Wiley  (Scopus  (CrossRef (Scopus information is found. [need login])
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(必須): 1591 1603 [継承]
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年月日 (必須): 西暦 2018年 0月 初日 (平成 30年 0月 初日) [継承]
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DOI (任意): 10.1002/jcb.26319    (→Scopusで検索) [継承]
PMID (任意): 28771806    (→Scopusで検索) [継承]
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備考 (任意): 1.(英) PublicationType: Journal Article  (日)    [継承]

標準的な表示

和文冊子 ● Yuka Hiroshima, Eijiro Sakamoto, Kaya Yoshida, Kaori Abe, Koji Naruishi, Takenori Yamamoto, Yasuo Shinohara, Jun-ichi Kido and Carolyn L Geczy : Advanced glycation end-products and Porphyromonas gingivalis lipopolysaccharide increase calprotectin expression in human gingival epithelial cells., Journal of Cellular Biochemistry, Vol.119, No.2, 1591-1603, 2018.
欧文冊子 ● Yuka Hiroshima, Eijiro Sakamoto, Kaya Yoshida, Kaori Abe, Koji Naruishi, Takenori Yamamoto, Yasuo Shinohara, Jun-ichi Kido and Carolyn L Geczy : Advanced glycation end-products and Porphyromonas gingivalis lipopolysaccharide increase calprotectin expression in human gingival epithelial cells., Journal of Cellular Biochemistry, Vol.119, No.2, 1591-1603, 2018.

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