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  1. 20 医学系研究科・医学部
  2. 20F 学位論文
  3. 20F1 博士論文
  4. H27年度 (20F1)

G-protein-coupled estrogen recepter agonist suppresses airway inflammation in a mouse model of asthma through IL-10

http://hdl.handle.net/10295/2965
http://hdl.handle.net/10295/2965
9023512d-0fb2-4f1c-955d-664dd41a991b
名前 / ファイル ライセンス アクション
ihakukouyoushi1139.pdf 内容要旨及び審査結果要旨 (844.7 kB)
ihakukou1139.pdf 本文 (241.1 kB)
Item type 学位論文 / Thesis or Dissertation(1)
公開日 2015-12-04
タイトル
タイトル G-protein-coupled estrogen recepter agonist suppresses airway inflammation in a mouse model of asthma through IL-10
言語
言語 jpn
資源タイプ
資源タイプ識別子 http://purl.org/coar/resource_type/c_db06
資源タイプ doctoral thesis
アクセス権
アクセス権 open access
アクセス権URI http://purl.org/coar/access_right/c_abf2
別タイトル
その他のタイトル G 蛋白共役エストロゲン受容体アゴニストは喘息モデルマウスに対して IL-10 を介し気道炎症を抑制する
作成者 糸賀, 正道

× 糸賀, 正道

糸賀, 正道

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ITOGA, Masamichi

× ITOGA, Masamichi

en ITOGA, Masamichi

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内容記述(抄録)
内容記述タイプ Other
内容記述 Estrogen influences the disease severity and sexual dimorphism in asthma, which
is caused by complex mechanisms. Besides classical nuclear estrogen receptors (ERα/β),
G-protein-coupled estrogen receptor (GPER) was recently established as an estrogen
receptor on the cell membrane. Although GPER is associated with immunoregulatory
functions of estrogen, the pathophysiological role of GPER in allergic inflammatory
lung disease has not been examined. We investigated the effect of GPER-specific
agonist G-1 in asthmatic mice. GPER expression in asthmatic lung was confirmed by
immunofluorescent staining. OVA-sensitized BALB/c and C57BL/6 mice were treated
with G-1 by daily subcutaneous injections during an airway challenge phase, followed
by histological and biochemical examination. Strikingly, administration of G-1
attenuated airway hyperresponsiveness, accumulation of inflammatory cells, and levels
of Th2 cytokines (IL-5 and IL-13) in BAL fluid. G-1 treatment also decreased serum
levels of anti-OVA IgE antibodies. The frequency of splenic Foxp3+CD4+ regulatory T
cells and IL-10-producing GPER+CD4+ T cells was significantly increased in
G-1-treated mice. Additionally, splenocytes isolated from G-1-treated mice showed
greater IL-10 production. G-1-induced amelioration of airway inflammation and IgE
production were abolished in IL-10-deficient mice. Taken together, these results
indicate that extended GPER activation negatively regulates the acute asthmatic
condition by altering the IL-10-producing lymphocyte population. The current results
have potential importance for understanding the mechanistic aspects of function of
estrogen in allergic inflammatory response.
著者版フラグ
出版タイプ VoR
出版タイプResource http://purl.org/coar/version/c_970fb48d4fbd8a85
書誌情報 発行日 2015-11-01
出版者
出版者 秋田大学
備考
秋田大学審査学位論文(PLoS ONE,10(8)掲載論文)
学位名
学位名 博士(医学)
学位授与機関
学位授与機関識別子Scheme kakenhi
学位授与機関識別子 11401
学位授与機関名 秋田大学
学位授与年月日
学位授与年月日 2015-09-24
学位授与番号
学位授与番号 甲第1139号
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