Open Access

miR-30a attenuates cardiac fibrosis in rats with myocardial infarction by inhibiting CTGF

  • Authors:
    • Liwen Chen
    • Qian Ji
    • Hao Zhu
    • Yizhi Ren
    • Zhongguo Fan
    • Nailiang Tian
  • View Affiliations

  • Published online on: March 13, 2018     https://doi.org/10.3892/etm.2018.5952
  • Pages: 4318-4324
  • Copyright: © Chen et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

The mechanism of miR-30a in myocardial fibrosis in rats with myocardial infarction (MI) was investigated. rAAV9-miR-30a was constructed and transfected to heart via injecting into the left ventricular cavity of MI rats. The sham operation group, control group, miR-30a group and miR‑30a-NC group were established. Besides, the 3'-UTR of CTGF was inserted into luciferase expression plasmid (pMir‑report), then transfected into COS1 cells. miR-30a and control miRNA were, respectively, cotransfected into COS1 cells. The expression of luciferase was detected before and after knockdown of the binding site of miR-30a and the 3'-UTR of CTGF. Four weeks after MI surgery, cardiac function was measured by color Doppler echocardiography, including short axis shortening (FS) and left ventricular ejection fraction (LVEF); the myocardial collagen volume fraction (CVF) was observed by Masson's staining; deposition of collagen I and collagen III were evaluated by immunohistochemical stain; using real-time PCR to detect expression levels of miR-30a and CTGF; the expression of CTGF was observed by western blotting. In MI group, cardiac function was significantly improved, while the expression levels of CVF, collagen I and III, the ratio of type I/III collagen, CTGF were significantly reduced. After knockdown the binding site of miR-30a and the 3'-UTR of CTGF, luciferase expression in COS1 cells decreased significantly. miR-30a might inhibit the expression of CTGF by directly combining with the 3'-UTR site of CTGF after MI, thereby reduce the production of collagen in myocardia, inhibit myocardial fibrosis, then improve cardiac function.
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May-2018
Volume 15 Issue 5

Print ISSN: 1792-0981
Online ISSN:1792-1015

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Copy and paste a formatted citation
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Spandidos Publications style
Chen L, Ji Q, Zhu H, Ren Y, Fan Z and Tian N: miR-30a attenuates cardiac fibrosis in rats with myocardial infarction by inhibiting CTGF. Exp Ther Med 15: 4318-4324, 2018
APA
Chen, L., Ji, Q., Zhu, H., Ren, Y., Fan, Z., & Tian, N. (2018). miR-30a attenuates cardiac fibrosis in rats with myocardial infarction by inhibiting CTGF. Experimental and Therapeutic Medicine, 15, 4318-4324. https://doi.org/10.3892/etm.2018.5952
MLA
Chen, L., Ji, Q., Zhu, H., Ren, Y., Fan, Z., Tian, N."miR-30a attenuates cardiac fibrosis in rats with myocardial infarction by inhibiting CTGF". Experimental and Therapeutic Medicine 15.5 (2018): 4318-4324.
Chicago
Chen, L., Ji, Q., Zhu, H., Ren, Y., Fan, Z., Tian, N."miR-30a attenuates cardiac fibrosis in rats with myocardial infarction by inhibiting CTGF". Experimental and Therapeutic Medicine 15, no. 5 (2018): 4318-4324. https://doi.org/10.3892/etm.2018.5952