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    MicroRNA-210-mediated proliferation, survival, and angiogenesis promote cardiac repair post myocardial infarction in rodents

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    File Available After 12/01/2018 (1.804Mb)
    Issue Date
    2017-12
    Author
    Arif, Mohammed
    Pandey, Raghav
    Alam, Perwez
    Jiang, Shujia
    Sadayappan, Sakthivel
    Paul, Arghya
    Ahmed, Rafeeq P. H.
    Publisher
    Springer Verlag
    Type
    Article
    Article Version
    Scholarly/refereed, publisher version
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    Abstract
    An innovative approach for cardiac regeneration following injury is to induce endogenous cardiomyocyte (CM) cell cycle re-entry. In the present study, CMs from adult rat hearts were isolated and transfected with cel-miR-67 (control) and rno-miR-210. A significant increase in CM proliferation and mono-nucleation were observed in miR-210 group, in addition to a reduction in CM size, multi-nucleation, and cell death. When compared to control, β-catenin and Bcl-2 were upregulated while APC (adenomatous polyposis coli), p16, and caspase-3 were downregulated in miR-210 group. In silico analysis predicted cell cycle inhibitor, APC, as a direct target of miR-210 in rodents. Moreover, compared to control, a significant increase in CM survival and proliferation were observed with siRNA-mediated inhibition of APC. Furthermore, miR-210 overexpressing C57BL/6 mice (210-TG) were used for short-term ischemia/reperfusion study, revealing smaller cell size, increased mono-nucleation, decreased multi-nucleation, and increased CM proliferation in 210-TG hearts in contrast to wild-type (NTG). Likewise, myocardial infarction (MI) was created in adult mice, echocardiography was performed, and the hearts were harvested for immunohistochemistry and molecular studies. Compared to NTG, 210-TG hearts showed a significant increase in CM proliferation, reduced apoptosis, upregulated angiogenesis, reduced infarct size, and overall improvement in cardiac function following MI. β-catenin, Bcl-2, and VEGF (vascular endothelial growth factor) were upregulated while APC, p16, and caspase-3 were downregulated in 210-TG hearts. Overall, constitutive overexpression of miR-210 rescues heart function following cardiac injury in adult mice via promoting CM proliferation, cell survival, and angiogenesis.
    Description
    The final publication is available at Springer via http://dx.doi.org/10.1007/s00109-017-1591-8.
    URI
    http://hdl.handle.net/1808/26461
    DOI
    https://doi.org/10.1007/s00109-017-1591-8
    Collections
    • Chemical & Petroleum Engineering Scholarly Works [173]
    Citation
    Arif, M., Pandey, R., Alam, P., Jiang, S., Sadayappan, S., Paul, A., & Ahmed, R. P. H. (2017). MicroRNA-210-mediated proliferation, survival, and angiogenesis promote cardiac repair post myocardial infarction in rodents. Journal of Molecular Medicine (Berlin, Germany), 95(12), 1369–1385. http://doi.org/10.1007/s00109-017-1591-8

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    KU Libraries
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    785-864-8983

    KU Libraries
    1425 Jayhawk Blvd
    Lawrence, KS 66045
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    Contact KU ScholarWorks
    785-864-8983
    KU Libraries
    1425 Jayhawk Blvd
    Lawrence, KS 66045
    785-864-8983

    KU Libraries
    1425 Jayhawk Blvd
    Lawrence, KS 66045
    Image Credits
     

     

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