Acute myocardial infarction induced functional cardiomyocytes to re-enter the cell cycle

Yongjun Li, Shengda Hu, Genshan Ma*, Yuyu Yao, Gaoliang Yan, Jia Chen, Yefei Li, Zhuoli Zhang

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

14 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)327-335
Number of pages9
JournalAmerican Journal of Translational Research
Volume5
Issue number3
StatePublished - 2013

Keywords

  • Acute myocardial infarction
  • Cell cycle
  • Cyclin A2
  • Mitosis

ASJC Scopus subject areas

  • Molecular Medicine
  • Clinical Biochemistry
  • Cancer Research

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