フルテキストファイル
著者
Ono Kimiyo Second Department of Surgery, Faculty of Medicine, Tottori University
Ishiguro Shingo Second Department of Surgery, Faculty of Medicine, Tottori University
Kuroda Hiroaki Second Department of Surgery, Faculty of Medicine, Tottori University
Ohgi Shigetsugu Second Department of Surgery, Faculty of Medicine, Tottori University KAKEN
キーワード
annexin V
apoptosis
cardiomyocyte
phosphatidylserine
reoxygenation injury
抄録
Ischemia/reperfusion injury plays a crucial role in the induction of the cell death of myocytes. The precise mechanism of the cell death, however, has not been elucidated enough. This study examined the cell death of rat neonatal myocytes induced by chemical ischemia and reoxygenation with an in vitro model, in terms of apoptosis, and the role of phosphatidylserine, which is recognized with annexin V. Chemical ischemia and reoxygenation were conducted on the cultured myocytes obtained from 1- or 2-day-old Wistar rats. The cells were divided into 4 groups exposed to chemical ischemia for 9 h (Group A), 18 h (Group B) and 24 h (Group C) and one group not exposed to chemical ischemia (Control Group). DNA ladder formation on agarose gel electrophoresis was noted in Groups B and C followed by reoxygenation, but not in Group A, as well as all 4 groups without reoxygenation. There were cells positive to terminal deoxynucleotidyl transferase-mediated dUDP-biotin nick end labeling in all 3 groups except for the Control Group; after reoxygenation, the number of cells became larger in Groups B and C than in Group A. Flow cytometry revealed that annexin V-positive cells were 1.15 ± 0.82% in the Control Group, 4.07 ± 3.8% in Group A without reoxygenation and 15.5 ± 6.3% in Group A after 30-min reoxygenation, respectively; the value was significantly higher in the latter than the former two (P < 0.01). Although 18-h and 24-h ischemia increased the annexin V-positive cells, reoxygenation did not alter the number of cells in Groups B and C. These results indicate that i) chemical ischemia followed by reoxygenation variably induces apoptosis of rat myocytes, ii) long-term ischemia causes phosphatidylserine translocation on the cell surface membrane, regardless of reoxygenation and iii) mild ischemia necessitates reoxygenation to translocate phosphatidylserine, which might play a crucial role in the initiation of apoptosis of the myocytes.
出版者
Tottori University Faculty of Medicine
資料タイプ
学術雑誌論文
ISSN
1346-8049
書誌ID
AA00892882
掲載誌名
Yonago Acta medica
最新掲載誌名
Yonago Acta medica
43
1
開始ページ
11
終了ページ
18
発行日
2000-03
著者版フラグ
出版社版
著作権表記
Yonago Acta medica 編集委員会
掲載情報
Yonago Acta medica. 2000, 43(1), 11-18
部局名
医学部・医学系研究科・医学部附属病院
言語
英語