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Article

miR-483-3p regulates acute myocardial infarction by transcriptionally repressing insulin growth factor 1 expression

  • Authors:
    • Hao Sun
    • Jun Cai
    • Li Xu
    • Jiamei Liu
    • Mulei Chen
    • Meili Zheng
    • Lefeng Wang
    • Xinchun Yang
  • View Affiliations / Copyright

    Affiliations: Heart Center, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, P.R. China
  • Pages: 4785-4790
    |
    Published online on: January 18, 2018
       https://doi.org/10.3892/mmr.2018.8456
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Abstract

The aim of the present study was to evaluate the functional association between the expression of miR‑483‑3p and acute myocardial infarction (AMI) in patients and in vitro. H9c2 cells were incubated in a vacuum with 5% CO2, 5% H2 and 90% N2 for 2 h, which generated the AMI model in vitro. Reverse transcription‑quantitative polymerase chain reaction was used to measure miR‑483‑3p expression, and flow cytometry analysis and ELISA analysis were used to analyze apoptosis rate via caspase‑3 and caspase‑9 activity kits. B‑cell lymphoma 2 (Bcl‑2)/Bcl‑2‑associated X protein (Bax) and transcriptionally suppressed the protein expression of insulin growth factor 1 (IGF‑1) were analyze using western blot analysis. The results demonstrated that the expression of miR‑483‑3p in patients with AMI was increased when compared with the control group. In the in vitro model, the overexpression of miR‑483‑3p promoted apoptosis, increased caspase‑3 and caspase‑9 activity levels, induced the protein expression of Bcl‑2/Bax and IGF‑1. Picropodophyllotoxin, an IGF‑1 inhibitor, was administered to cells following the overexpression of miR‑483‑3p. Administration of picropodophyllotoxin suppressed IGF‑1 protein expression, promoted apoptosis, increased caspase‑3 and caspase‑9 activity levels, and induced the protein expression of Bax/Bcl‑2. The results of the present study revealed that miR‑483‑3p may regulate AMI via the IGF‑1 signaling pathway and may support the restoration of functional performance following AMI.
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Copy and paste a formatted citation
Spandidos Publications style
Sun H, Cai J, Xu L, Liu J, Chen M, Zheng M, Wang L and Yang X: miR-483-3p regulates acute myocardial infarction by transcriptionally repressing insulin growth factor 1 expression. Mol Med Rep 17: 4785-4790, 2018.
APA
Sun, H., Cai, J., Xu, L., Liu, J., Chen, M., Zheng, M. ... Yang, X. (2018). miR-483-3p regulates acute myocardial infarction by transcriptionally repressing insulin growth factor 1 expression. Molecular Medicine Reports, 17, 4785-4790. https://doi.org/10.3892/mmr.2018.8456
MLA
Sun, H., Cai, J., Xu, L., Liu, J., Chen, M., Zheng, M., Wang, L., Yang, X."miR-483-3p regulates acute myocardial infarction by transcriptionally repressing insulin growth factor 1 expression". Molecular Medicine Reports 17.3 (2018): 4785-4790.
Chicago
Sun, H., Cai, J., Xu, L., Liu, J., Chen, M., Zheng, M., Wang, L., Yang, X."miR-483-3p regulates acute myocardial infarction by transcriptionally repressing insulin growth factor 1 expression". Molecular Medicine Reports 17, no. 3 (2018): 4785-4790. https://doi.org/10.3892/mmr.2018.8456
Copy and paste a formatted citation
x
Spandidos Publications style
Sun H, Cai J, Xu L, Liu J, Chen M, Zheng M, Wang L and Yang X: miR-483-3p regulates acute myocardial infarction by transcriptionally repressing insulin growth factor 1 expression. Mol Med Rep 17: 4785-4790, 2018.
APA
Sun, H., Cai, J., Xu, L., Liu, J., Chen, M., Zheng, M. ... Yang, X. (2018). miR-483-3p regulates acute myocardial infarction by transcriptionally repressing insulin growth factor 1 expression. Molecular Medicine Reports, 17, 4785-4790. https://doi.org/10.3892/mmr.2018.8456
MLA
Sun, H., Cai, J., Xu, L., Liu, J., Chen, M., Zheng, M., Wang, L., Yang, X."miR-483-3p regulates acute myocardial infarction by transcriptionally repressing insulin growth factor 1 expression". Molecular Medicine Reports 17.3 (2018): 4785-4790.
Chicago
Sun, H., Cai, J., Xu, L., Liu, J., Chen, M., Zheng, M., Wang, L., Yang, X."miR-483-3p regulates acute myocardial infarction by transcriptionally repressing insulin growth factor 1 expression". Molecular Medicine Reports 17, no. 3 (2018): 4785-4790. https://doi.org/10.3892/mmr.2018.8456
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