WEKO3
インデックスリンク
アイテム
Postinfarction Cardiac Remodeling Normally Proceeds in Granulocyte Colony-Stimulating Factor Knockout Mice.
https://asahi-u.repo.nii.ac.jp/records/2363
https://asahi-u.repo.nii.ac.jp/records/236322e84469-b702-4175-8001-a51053092932
| Item type | 朝日大学 教育・研究業績(1) | |||||
|---|---|---|---|---|---|---|
| 公開日 | 2015-02-20 | |||||
| タイトル | ||||||
| タイトル | Postinfarction Cardiac Remodeling Normally Proceeds in Granulocyte Colony-Stimulating Factor Knockout Mice. | |||||
| 言語 | ||||||
| 言語 | eng | |||||
| 資源タイプ | ||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_1843 | |||||
| 資源タイプ | other | |||||
| アクセス権 | ||||||
| アクセス権 | metadata only access | |||||
| アクセス権URI | http://purl.org/coar/access_right/c_14cb | |||||
| 業績分類 | ||||||
| 値 | 学会発表 | |||||
| 教員氏名 |
竹村, 元三
× 竹村, 元三 |
|||||
| 発行、発表雑誌等、又は発表学会等の名称 | ||||||
| 値 | 第78回日本循環器学会総会・学術集会（東京） | |||||
| 単著、共著の別 | ||||||
| 値 | 共同 | |||||
| 発行又は発表の年月 | ||||||
| 日付 | 2014-03-21 | |||||
| 概要 | ||||||
| 値 | Treatment with granulocyte colony-stimulating factor (G-CSF) has been reported to mitigate postinfarction cardiac remodeling. We here examined how the postinfarction remodeling processes in the hearts of G-CSF-null mice, of which outcome we hypothesized to be miserable. We generated myocardial infarction in G-CSF-knockout (KO) mice and wild-type (WT) mice by ligation of the left coronary artery. Somewhat surprisingly, at the chronic stage (4 weeks postinfarction), there was no difference in the left ventricular dimension, function and histological findings including the infarct size and myocardial vascular density between the groups. Biochemical analyses revealed a markedly increased expression of vascular endothelial growth factor (VEGF) in the hearts of KO mice compared with WT mice. When KO mice were treated with an anti-VEGF antibody bevacizumab, the cardiac remodeling was significantly aggravated at the chronic stage, where the infarct wall was thinner and vascular density was fewer. In the granulation tissue of the bevacizumab-treated hearts at the subacute stage (4 days postinfarction), scarce vascular development, reduced cell proliferation activity, and increased apoptosis were noted, which might have contributed to the aggravation of cardiac remodeling during the chronic stage. In conclusion, G-CSF-KO mice unexpectedly displayed normal process of postinfarction cardiac remodeling. Overexpressed VEGF in the KO mice is suggested to compensate for the deficit of G-CSF through enhancement of neovascularization in the postinfarction heart. | |||||
