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Article

MicroRNA-26a protects against cardiac hypertrophy via inhibiting GATA4 in rat model and cultured cardiomyocytes

  • Authors:
    • Yan Liu
    • Zhiqian Wang
    • Wenliang Xiao
  • View Affiliations / Copyright

    Affiliations: Department of Cardiology, The Third Hospital of Hebei Medical University, Shijiazhuang, Hebei 050051, P.R. China
  • Pages: 2860-2866
    |
    Published online on: July 28, 2016
       https://doi.org/10.3892/mmr.2016.5574
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Abstract

Pathological cardiac hypertrophy is characterized by deleterious changes developed in cardiovascular diseases, whereas microRNAs (miRNAs) are involved in the mediation of cardiac hypertrophy. To investigate the role of microRNA-26a (miR-26a) in regulating cardiac hypertrophy and its functioning mechanisms, overexpression and suppression of miR‑26a via its mimic and inhibitor in a transverse abdominal aortic constriction (TAAC)-induced rat model and in angiotensin II (Ang II)-induced cardiomyocytes (CMs) was performed. In the rat model, the heart weight (HW) compared with the body weight (BW), the CM area, and expression of the hypertrophy‑associated factors, atrial natriuretic factor (ANF) and β‑myosin heavy chain (β‑MHC), were assessed. In CMs, the protein synthesis rate was determined using a leucine incorporation assay. Mutation of the GATA‑binding protein 4 (GATA4) 3'‑untranslated region (UTR) and overexpression of GATA4 were performed to confirm whether GATA4 is the target of miR‑26a. The results indicated that miR-26a was significantly downregulated in the heart tissue of the rat model, as well as in Ang II‑induced CMs (P<0.05). The TAAC-induced rat model exhibited a higher HW/BW ratio, a larger CM area, and higher expression levels of ANF and β‑MHC. CMs, upon Ang II treatment, also demonstrated a larger CM area, higher levels of ANF and β‑MHC, as well as accelerated protein synthesis. miR‑26a was not able to regulate GATA4 with mutations in the 3'‑UTR, indicating that GATA4 was the direct target of miR‑26a. Overexpression of GATA4 abrogated the inhibitory functions of miR‑26a in cardiac hypertrophy. Taken together, the present study suggested an anti‑hypertrophic role of miR‑26a in cardiac hypertrophy, possibly via inhibition of GATA4. These findings may be useful in terms of facilitating cardiac treatment, with potential therapeutic targets and strategies.
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Copy and paste a formatted citation
Spandidos Publications style
Liu Y, Wang Z and Xiao W: MicroRNA-26a protects against cardiac hypertrophy via inhibiting GATA4 in rat model and cultured cardiomyocytes. Mol Med Rep 14: 2860-2866, 2016.
APA
Liu, Y., Wang, Z., & Xiao, W. (2016). MicroRNA-26a protects against cardiac hypertrophy via inhibiting GATA4 in rat model and cultured cardiomyocytes. Molecular Medicine Reports, 14, 2860-2866. https://doi.org/10.3892/mmr.2016.5574
MLA
Liu, Y., Wang, Z., Xiao, W."MicroRNA-26a protects against cardiac hypertrophy via inhibiting GATA4 in rat model and cultured cardiomyocytes". Molecular Medicine Reports 14.3 (2016): 2860-2866.
Chicago
Liu, Y., Wang, Z., Xiao, W."MicroRNA-26a protects against cardiac hypertrophy via inhibiting GATA4 in rat model and cultured cardiomyocytes". Molecular Medicine Reports 14, no. 3 (2016): 2860-2866. https://doi.org/10.3892/mmr.2016.5574
Copy and paste a formatted citation
x
Spandidos Publications style
Liu Y, Wang Z and Xiao W: MicroRNA-26a protects against cardiac hypertrophy via inhibiting GATA4 in rat model and cultured cardiomyocytes. Mol Med Rep 14: 2860-2866, 2016.
APA
Liu, Y., Wang, Z., & Xiao, W. (2016). MicroRNA-26a protects against cardiac hypertrophy via inhibiting GATA4 in rat model and cultured cardiomyocytes. Molecular Medicine Reports, 14, 2860-2866. https://doi.org/10.3892/mmr.2016.5574
MLA
Liu, Y., Wang, Z., Xiao, W."MicroRNA-26a protects against cardiac hypertrophy via inhibiting GATA4 in rat model and cultured cardiomyocytes". Molecular Medicine Reports 14.3 (2016): 2860-2866.
Chicago
Liu, Y., Wang, Z., Xiao, W."MicroRNA-26a protects against cardiac hypertrophy via inhibiting GATA4 in rat model and cultured cardiomyocytes". Molecular Medicine Reports 14, no. 3 (2016): 2860-2866. https://doi.org/10.3892/mmr.2016.5574
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