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Article

Inactivation of INK4a and ARF induces myocardial proliferation and improves cardiac repair following ischemia‑reperfusion

  • Authors:
    • Songtao An
    • Yan Chen
    • Chuanyu Gao
    • Bingyu Qin
    • Xianhui Du
    • Fanmin Meng
    • Yanyan Qi
  • View Affiliations / Copyright

    Affiliations: Department of Cardiology, People's Hospital of Zhengzhou University, Zhengzhou, Henan 450003, P.R. China, Department of Anesthesia, People's Hospital of Zhengzhou University, Zhengzhou, Henan 450003, P.R. China
  • Pages: 5911-5916
    |
    Published online on: July 29, 2015
       https://doi.org/10.3892/mmr.2015.4133
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Abstract

The growth of the heart during mammalian embryonic development is primarily dependent on an increase in the number of cardiomyocytes (CM). However, shortly following birth, CMs cease proliferating and further growth of the myocardium is achieved via hypertrophic expansion of the existing CM population. The cyclin-dependent kinase inhibitor 2A (Cdkn2a) locus encodes overlapping genes for two tumor suppressor proteins, p16INK4a and p19 alternative reading frame (ARF). To determine whether decreased Cdkn2a gene expression results in improved cardiac regeneration in vitro and in vivo following cardiac injury, the proliferation of CMs isolated from Cdkn2a knockout (KO) and wild‑type (WT) mice in vitro and in vivo were evaluated following generation of ischemia reperfusion (IR) injury. The KO mice demonstrated enhanced CM proliferation not only in vitro, but also in vivo. Furthermore, heart function was improved and scar size was decreased in the KO mice compared with that of the WT mice. The results also indicated that microRNA (miR)‑1 and miR‑195 expression levels associated with cell proliferation were reduced following IR injury in KO mice compared with those of WT mice. These results suggested that the inactivation of INK4a and ARF stimulated CM proliferation and promoted cardiac repair.
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Copy and paste a formatted citation
Spandidos Publications style
An S, Chen Y, Gao C, Qin B, Du X, Meng F and Qi Y: Inactivation of INK4a and ARF induces myocardial proliferation and improves cardiac repair following ischemia‑reperfusion. Mol Med Rep 12: 5911-5916, 2015.
APA
An, S., Chen, Y., Gao, C., Qin, B., Du, X., Meng, F., & Qi, Y. (2015). Inactivation of INK4a and ARF induces myocardial proliferation and improves cardiac repair following ischemia‑reperfusion. Molecular Medicine Reports, 12, 5911-5916. https://doi.org/10.3892/mmr.2015.4133
MLA
An, S., Chen, Y., Gao, C., Qin, B., Du, X., Meng, F., Qi, Y."Inactivation of INK4a and ARF induces myocardial proliferation and improves cardiac repair following ischemia‑reperfusion". Molecular Medicine Reports 12.4 (2015): 5911-5916.
Chicago
An, S., Chen, Y., Gao, C., Qin, B., Du, X., Meng, F., Qi, Y."Inactivation of INK4a and ARF induces myocardial proliferation and improves cardiac repair following ischemia‑reperfusion". Molecular Medicine Reports 12, no. 4 (2015): 5911-5916. https://doi.org/10.3892/mmr.2015.4133
Copy and paste a formatted citation
x
Spandidos Publications style
An S, Chen Y, Gao C, Qin B, Du X, Meng F and Qi Y: Inactivation of INK4a and ARF induces myocardial proliferation and improves cardiac repair following ischemia‑reperfusion. Mol Med Rep 12: 5911-5916, 2015.
APA
An, S., Chen, Y., Gao, C., Qin, B., Du, X., Meng, F., & Qi, Y. (2015). Inactivation of INK4a and ARF induces myocardial proliferation and improves cardiac repair following ischemia‑reperfusion. Molecular Medicine Reports, 12, 5911-5916. https://doi.org/10.3892/mmr.2015.4133
MLA
An, S., Chen, Y., Gao, C., Qin, B., Du, X., Meng, F., Qi, Y."Inactivation of INK4a and ARF induces myocardial proliferation and improves cardiac repair following ischemia‑reperfusion". Molecular Medicine Reports 12.4 (2015): 5911-5916.
Chicago
An, S., Chen, Y., Gao, C., Qin, B., Du, X., Meng, F., Qi, Y."Inactivation of INK4a and ARF induces myocardial proliferation and improves cardiac repair following ischemia‑reperfusion". Molecular Medicine Reports 12, no. 4 (2015): 5911-5916. https://doi.org/10.3892/mmr.2015.4133
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