本資料は、掲載誌(URI)等のリンク先にある学位授与機関のWebサイトやCiNii Dissertationsから、本文を自由に閲覧できる場合があります。
博士論文
国立国会図書館館内限定公開
収録元データベースで確認する
国立国会図書館デジタルコレクション
デジタルデータあり
公開元のウェブサイトで確認する
DOI[info:doi/10.1371/journal.pone.0187894]のデータに遷移します
Apoptosis inhibitor of macrophage depletion decreased M1 macrophage accumulation and the incidence of cardiac rupture after myocardial infarction in mice
- 国立国会図書館永続的識別子
- info:ndljp/pid/11122658
国立国会図書館での利用に関する注記
資料に関する注記
一般注記:
- BackgroundCardiac rupture is an important cause of death in the acute phase after myocardial infarction (MI). Macrophages play a pivotal role in cardi...
書店で探す
書店で探す
書誌情報
この資料の詳細や典拠(同じ主題の資料を指すキーワード、著者名)等を確認できます。
デジタル
- 資料種別
- 博士論文
- 著者・編者
- 石川, 昇平
- 著者標目
- 出版年月日等
- 2018-03-24
- 出版年(W3CDTF)
- 2018-03-24
- 授与機関名
- 香川大学
- 授与年月日
- 2018-03-24
- 授与年月日(W3CDTF)
- 2018-03-24
- 報告番号
- 甲第689号
- 学位
- 博士(医学)
- 博論授与番号
- 甲第689号
- 本文の言語コード
- eng
- 著者別名
- 対象利用者
- 一般
- 一般注記
- BackgroundCardiac rupture is an important cause of death in the acute phase after myocardial infarction (MI). Macrophages play a pivotal role in cardiac remodeling after MI. Apoptosis inhibitor of macrophage (AIM) is secreted specifically by macrophages and contributes to macrophage accumulation in inflamed tissue by maintaining survival and recruiting macrophages. In this study, we evaluated the role of AIM in macrophage accumulation in the infarcted myocardium and cardiac rupture after MI.Methods and resultsWild-type (WT) and AIM‒/‒ mice underwent permanent left coronary artery ligation and were followed-up for 7 days. Macrophage accumulation and phenotypes (M1 pro-inflammatory macrophage or M2 anti-inflammatory macrophage) were evaluated by immunohistological analysis and RT-PCR. Matrix metalloproteinase (MMP) activity levels were measured by gelatin zymography. The survival rate was significantly higher (81.1% vs. 48.2%, P<0.05), and the cardiac rupture rate was significantly lower in AIM‒/‒ mice than in WT mice (10.8% vs. 31.5%, P<0.05). The number of M1 macrophages and the expression levels of M1 markers (iNOS and IL-6) in the infarcted myocardium were significantly lower in AIM‒/‒ mice than in WT mice. In contrast, there was no difference in the number of M2 macrophages and the expression of M2 markers (Arg-1, CD206 and TGF-β1) between the two groups. The ratio of apoptotic macrophages in the total macrophages was significantly higher in AIM‒/‒ mice than in WT mice, although MCP-1 expression did not differ between the two groups. MMP-2 and 9 activity levels in the infarcted myocardium were significantly lower in AIM‒/‒ mice than in WT mice.ConclusionsThese findings suggest that AIM depletion decreases the levels of M1 macrophages, which are a potent source of MMP-2 and 9, in the infarcted myocardium in the acute phase after MI by promoting macrophage apoptosis, and leads to a decrease in the incidence of cardiac rupture and improvements in survival rates.
- DOI
- info:doi/10.1371/journal.pone.0187894
- 国立国会図書館永続的識別子
- info:ndljp/pid/11122658
- コレクション(個別)
- 国立国会図書館デジタルコレクション > デジタル化資料 > 博士論文
- 収集根拠
- 博士論文(自動収集)
- 受理日(W3CDTF)
- 2018-08-03T23:36:01+09:00
- 作成日(W3CDTF)
- 2020-10-27
- 記録形式(IMT)
- PDF
- オンライン閲覧公開範囲
- 国立国会図書館内限定公開
- デジタル化資料送信
- 図書館・個人送信対象外
- 遠隔複写可否(NDL)
- 可
- 連携機関・データベース
- 国立国会図書館 : 国立国会図書館デジタルコレクション