ES cells overexpressing microRNA-1 attenuate apoptosis in the injured myocardium

    Authors

    C. Glass;D. K. Singla

    Comments

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    Abbreviated Journal Title

    Mol. Cell. Biochem.

    Keywords

    Apoptosis; Heart; microRNA; Akt; PTEN; EMBRYONIC STEM-CELLS; INHIBIT APOPTOSIS; PROGENITOR CELLS; GROWTH-FACTORS; H9C2 CELLS; DIFFERENTIATION; INFARCTION; HEART; EXPRESSION; REPAIR; Cell Biology

    Abstract

    MicroRNAs (miRs) are small, single-stranded, noncoding RNA's involved in post-transcriptional negative gene regulation. Recent investigations have underscored the integral role of miRs in various biological processes including innate immunity, cell-cycle regulation, metabolism, differentiation, and cell death. In the present study, we overexpressed miR-1, a muscle-specific miR, in embryonic stem cells (miR-1-ES cells), transplanted them into the infarcted myocardium, and evaluated their impact on cardiac apoptosis and function. We provide evidence demonstrating reduced apoptosis following transplantation of miR-1-ES cells 4 weeks post-myocardial infarction as compared to respective controls assessed by TUNEL staining and a capsase-3 activity assay. Moreover, we show significant elevation in p-Akt levels and diminished PTEN levels in hearts transplanted with miR-1-ES cells as determined by enzyme-linked immunoassays. Finally, using echocardiography, we reveal mice receiving miR-1-ES cell transplantation post-myocardial infarction had significantly improved fractional shortening and ejection fraction compared with respective controls. Our data suggest transplanted miR-1-ES cells inhibit apoptosis, mediated through the PTEN/Akt pathway, leading to improved cardiac function in the infarcted myocardium.

    Journal Title

    Molecular and Cellular Biochemistry

    Volume

    357

    Issue/Number

    1-2

    Publication Date

    1-1-2011

    Document Type

    Article

    Language

    English

    First Page

    135

    Last Page

    141

    WOS Identifier

    WOS:000295941500015

    ISSN

    0300-8177

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