title: Acute myocardial infarction induced functional cardiomyocytes to re-enter the cell cycle.
abstract: BACKGROUND
  Loss of cardiomyocytes after myocardial infarction (MI) causes heart failure. In this study, we investigate whether the in situ cardiomyocytes can re-enter the cell cycle and to what extent cell division of cardiomyocytes occurs after acute MI (AMI) in rats.
  
  
  METHODS
  Sprague Dawley (SD) rats were used in this study; the left anterior descending coronary artery was ligated. At time points (3 days, 1 week, 2 weeks, 3 weeks, and 4 weeks) after the operation, five rats were euthanized, respectively. An additional five sham-operated rats serves as a control group and were euthanized at 3 days post-operation. The expressions of cyclin A2, Ki-67, phospho-histone H3 (H3P), and Aurora B in myocardial tissues were detected by Western blot and immunofluorescence.
  
  
  RESULTS
  The expression levels of cyclin A2 were significantly higher in all groups with AMI except the 4-week group than those found in the sham-operated group (P < 0.01). The percentage of Ki-67-positive nuclei in the border zones was significantly higher than the percentage in the distant normal myocardium (P < 0.01).
  
  
  CONCLUSIONS
  our results demonstrate that cardiomyocytes re-enter the cell cycle after AMI and that cyclin A2 is a reliable marker for the detection of cell cycle activity in cardiomyocytes.
authors: Department of Cardiology, Zhongda Hospital, Medical School of Southeast University Nanjing, China.
authors: Yongjun
authors: Y
authors: Li
authors: Shengda
authors: S
authors: Hu
authors: Genshan
authors: G
authors: Ma
authors: Yuyu
authors: Y
authors: Yao
authors: Gaoliang
authors: G
authors: Yan
authors: Jia
authors: J
authors: Chen
authors: Yefei
authors: Y
authors: Li
authors: Zhuoli
authors: Z
authors: Zhang
keywords: Acute myocardial infarction; cell cycle; cyclin A2; mitosis
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