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Am J Transl Res 2013;5(3):327-335
Original Article
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
Department of Cardiology, Zhongda Hospital, Medical School of Southeast University, Nanjing, China; RCIS, Cath
and EP Lab, Inova Fairfax Hospital, Virginia, USA; Department of Radiology, Northwestern University, Chicago,
USA; Equal contributors to this work.
Received March 7, 2013; Accepted March 29, 2013; Epub April 19, 2013; Published April 30, 2013
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. (AJTR1303005).
Keywords: Acute myocardial infarction, mitosis, cell cycle, cyclin A2
Address correspondence to: Dr. Genshan Ma, Department of Cardiology, Zhongda Hospital, Medical School of
Southeast University, NO. 87 Dingjiaqiao Road, Nanjing, Jiangsu 210009, China. Tel: 86-258-326-2391; Fax: 86-
258-326-2395; E-mail: magenshan@hotmail.com; Dr. Zhuoli Zhang, Department of Radiology, Northwestern
University, 737 N. Michigan Ave, 16th Floor, Chicago, IL 60611. Tel: 312-926-3874; Fax: 312-926-5991; E-mail:
zhuoli-zhang@northwestern.edu
Original Article
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
Department of Cardiology, Zhongda Hospital, Medical School of Southeast University, Nanjing, China; RCIS, Cath
and EP Lab, Inova Fairfax Hospital, Virginia, USA; Department of Radiology, Northwestern University, Chicago,
USA; Equal contributors to this work.
Received March 7, 2013; Accepted March 29, 2013; Epub April 19, 2013; Published April 30, 2013
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. (AJTR1303005).
Keywords: Acute myocardial infarction, mitosis, cell cycle, cyclin A2
Address correspondence to: Dr. Genshan Ma, Department of Cardiology, Zhongda Hospital, Medical School of
Southeast University, NO. 87 Dingjiaqiao Road, Nanjing, Jiangsu 210009, China. Tel: 86-258-326-2391; Fax: 86-
258-326-2395; E-mail: magenshan@hotmail.com; Dr. Zhuoli Zhang, Department of Radiology, Northwestern
University, 737 N. Michigan Ave, 16th Floor, Chicago, IL 60611. Tel: 312-926-3874; Fax: 312-926-5991; E-mail:
zhuoli-zhang@northwestern.edu
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