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Dysregulation of CD69 by overexpression of microRNA‑367‑3p associated with post‑myocardial infarction cardiac fibrosis

  • Authors:
    • Haiyan Hu
    • Jing Li
    • Jingfang Zhang

  • View Affiliations

  • Published online on: June 29, 2018     https://doi.org/10.3892/mmr.2018.9234
  • Pages: 3085-3092
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Abstract

Cardiac fibrosis is characterized as net accumulation of ECM (extracellular matrix) proteins in the cardiac interstitium, which contributes to dysfunction of both systolic and diastolic. The present study aimed to identify the association between microRNA (miR)‑367‑3p and cluster of differentiation 69 (CD69), and their roles in regulating the development of cardiac fibrosis. Participants (n=34) were enrolled and diagnosed with cardiac fibrosis [fibrosis (+); n=16] or non‑fibrosis control [fibrosis (‑); n=18]. In‑silicon analysis and luciferase assay were used to identify CD69 as a target of miR‑367‑3p. Reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) and western blot analysis were used to determine the expression level of miR‑367‑3p and CD69 mRNA and protein, in patient groups or cells transfected with miR‑367‑3p mimics or inhibitors. Cytokine assays were used to detect the level of interleukin (IL)‑17, tumor necrosis factor (TNF)‑α, interferon (IFN)‑γ and granulocyte macrophage colony‑stimulating factor. Flow cytometry was used to detect the T helper (Th)‑17 fraction of cells in different treatment groups. Analysis by RT‑qPCR indicated that the expression of miR‑367‑3p was decreased in the cardiac fibrosis (+) group compared with the fibrosis (‑) control group. In contrast, the level of CD69 mRNA was increased in the cardiac fibrosis group compared with the control group. The CD69 3'‑untranslated region (UTR) contained two potential seed regions for miR‑367‑3p and was therefore predicted as a target. A dual‑luciferase reporter assay demonstrated a reduced luciferase activity of cells transfected with wild‑type CD69 3'‑UTR and the mutant2 CD69 3'‑UTR, however, the mutant1 CD69 3'‑UTR completely abolished the interaction with miR‑367‑3p. Furthermore, the CD69 mRNA and protein expression levels in cells transfected with miR‑367‑3p mimics and CD69 siRNA were downregulated compared with the scramble control. Cytokine analysis demonstrated increased levels of IL‑17 and TNF‑α in cells transfected with miR‑367‑3p mimics or CD69 siRNA, compared with the scramble control. The IFN‑γ and GM‑CSF levels of cells transfected with pcDNA3‑CD69, miR‑367‑3p mimics or miR‑367‑3p + pcDNA3‑CD69 were comparable with the scramble control. Notably, the Th17 fraction of cells was upregulated following the introduction of miR‑367‑3p mimics or CD69 siRNA. In conclusion, these results provide evidence that a decrease in miR‑367‑3p levels may be associated with cardiac fibrosis.
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September-2018
Volume 18 Issue 3

Print ISSN: 1791-2997
Online ISSN:1791-3004

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  • Journal Metrics
  • Impact Factor: 3.4
  • Ranked Medicine Research and Experimental
    (total number of cites)
  • CiteScore: 7.6
  • CiteScore Rank: Q1: #82/347 Biochemistry, Genetics and Molecular Biology
  • Source Normalized Impact per Paper (SNIP): 0.647
  • SCImago Journal Rank (SJR): 0.781
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Spandidos Publications style
Hu H, Li J and Zhang J: Dysregulation of CD69 by overexpression of microRNA‑367‑3p associated with post‑myocardial infarction cardiac fibrosis. Mol Med Rep 18: 3085-3092, 2018
APA
Hu, H., Li, J., & Zhang, J. (2018). Dysregulation of CD69 by overexpression of microRNA‑367‑3p associated with post‑myocardial infarction cardiac fibrosis. Molecular Medicine Reports, 18, 3085-3092. https://doi.org/10.3892/mmr.2018.9234
MLA
Hu, H., Li, J., Zhang, J."Dysregulation of CD69 by overexpression of microRNA‑367‑3p associated with post‑myocardial infarction cardiac fibrosis". Molecular Medicine Reports 18.3 (2018): 3085-3092.
Chicago
Hu, H., Li, J., Zhang, J."Dysregulation of CD69 by overexpression of microRNA‑367‑3p associated with post‑myocardial infarction cardiac fibrosis". Molecular Medicine Reports 18, no. 3 (2018): 3085-3092. https://doi.org/10.3892/mmr.2018.9234