『徳島大学 教育・研究者情報データベース (EDB)』---[学外] /
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EID=298093EID:298093, Map:0, LastModified:2015年9月8日(火) 21:24:29, Operator:[大家 隆弘], 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]
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著者 (必須): 1. (英) Geczy Carolyn L (日) (読)
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2. (英) Chung Yuen Ming (日) (読)
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3.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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題名 (必須): (英) Calgranulins may contribute vascular protection in atherogenesis.  (日)    [継承]
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要約 (任意): (英)   (日) S100A8, S100A9 and S100A12 are considered proinflammatory mediators of atherosclerosis. Known as calgranulins, they are major components of neutrophils and are upregulated in macrophages and foam cells. They influence leukocyte recruitment, and may propagate inflammation by binding TLR4 and/or receptor for advanced glycation endproducts (RAGE). However, the receptors for calgranulins remain an enigma; we have no evidence for TLR4 or RAGE activation by S100A8 or S100A12. Moreover, gene regulation studies suggest antiinflammatory functions for S100A8 and emerging reports indicate pleiotropic roles. Unlike S100A9, S100A8 effectively scavenges oxidants generated by the myeloperoxidase system in vivo, forming novel thiol modifications. S100A8 is also readily S-nitrosylated, stabilizing nitric oxide and transporting it to hemoglobin. S100A8-SNO reduces leukocyte transmigration in the vasculature. S-glutathionylation of S100A9 modifies its effects on leukocyte adhesion. Both S100A8 forms inhibit mast cell activation, at least partially by scavenging reactive oxygen species required for signaling. Conversely, S100A12 activates and sequesters mast cells. However S100A12 suppresses proinflammatory cytokine induction by SAA-activated monocytes and macrophages, and inhibits matrix metalloprotease activity. We propose that the abundance and types of cells expressing calgranulins in particular microenvironments, their relative concentrations and post-translational modifications may have distinct functional outcomes, including those that are protective, at different stages of atherogenesis.   [継承]
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誌名 (必須): Circulation Journal ([社団法人 日本循環器学会])
(pISSN: 1346-9843, eISSN: 1347-4820)

ISSN (任意): 1347-4820
ISSN: 1346-9843 (pISSN: 1346-9843, eISSN: 1347-4820)
Title: Circulation journal : official journal of the Japanese Circulation Society
Title(ISO): Circ J
Supplier: 社団法人日本循環器学会
Publisher: Japanese Circulation Society/Nihon Junkanki Gakkai
 (NLM Catalog  (Webcat Plus  (医中誌Web  (J-STAGE  (Scopus  (CrossRef (Scopus information is found. [need login])
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年月日 (必須): 西暦 2013年 12月 27日 (平成 25年 12月 27日) [継承]
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DOI (任意): 10.1253/circj.CJ-13-1505    (→Scopusで検索) [継承]
PMID (任意): 24389598    (→Scopusで検索) [継承]
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備考 (任意): 1.(英) PublicationType: Journal Article  (日)    [継承]
2.(英) PublicationType: Research Support, Non-U.S. Gov't  (日)    [継承]
3.(英) PublicationType: Review  (日)    [継承]

標準的な表示

和文冊子 ● L Carolyn Geczy, Ming Yuen Chung and Yuka Hiroshima : Calgranulins may contribute vascular protection in atherogenesis., Circulation Journal, Vol.78, No.2, 271-280, 2013.
欧文冊子 ● L Carolyn Geczy, Ming Yuen Chung and Yuka Hiroshima : Calgranulins may contribute vascular protection in atherogenesis., Circulation Journal, Vol.78, No.2, 271-280, 2013.

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