Biotechnology Letters

, Volume 39, Issue 7, pp 967–976 | Cite as

Knockdown of microRNA-17-5p ameliorates atherosclerotic lesions in ApoE−/− mice and restores the expression of very low density lipoprotein receptor

  • Lili Tan
  • Liang Meng
  • Xiaojing Shi
  • Bo Yu
Original Research Paper



To propose and verify a hypothesis that miR-17-5p knockdown may mitigate atherosclerotic lesions using atherosclerotic ApoE−/− mice as serum microRNA-17-5p (miR-17-5p) is elevated in patients with atherosclerosis.


The level of miR-17-5p was higher while the level of very low density lipoprotein receptor (VLDLR), a predicted target of miR-17-5p, was lower in the peripheral blood lymphocytes (PBLs) of atherosclerosis patients as compared with control PBLs. ApoE−/− mice fed with a high-cholesterol diet displayed marked atherosclerotic vascular lesions, which were ameliorated after treatment with antagomiR-17-5p. Moreover, the decreased VLDLR in atherosclerotic mice was partly restored when miR-17-5p was antagonized. Further, luciferase assay confirmed VLDLR as a direct target of miR-17-5p in vascular smooth muscle cells (VSMCs). In addition, the elevated expression of proprotein convertase subtilisin kexin 9 (PCSK9), a secreted protease that binds to and promotes VLDLR degradation, in the atherosclerotic mice was suppressed by antagomiR-17-5p.


A novel interaction between miR-17-5p and VLDLR is revealed and suggests that miR-17-5p may be a potential therapeutic target for AS.


Atherosclerosis MicroRNA-17-5p Proprotein convertase subtilisin kexin 9 Very low density lipoprotein receptor 


Supporting information

Supplementary Table 1—Primer information used for RT-PCR analysis.

Supplementary Figure 1—The expression level of VLDLR after treatment with or without antagomiR-17-5p in the heart of atherosclerotic ApoE−/− mice by Western blot analysis.

Compliance with ethical standards

Conflict of interest

The authors declare no conflict of interest.

Supplementary material

10529_2017_2337_MOESM1_ESM.docx (17 kb)
Supplementary material 1 (DOCX 16 kb)
10529_2017_2337_MOESM2_ESM.tif (138 kb)
Supplementary material 2 (TIFF 137 kb)


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Copyright information

© Springer Science+Business Media Dordrecht 2017

Authors and Affiliations

  1. 1.Department of CardiologyThe First Affiliated Hospital of China Medical UniversityShenyangPeople’s Republic of China
  2. 2.Department of CardiologyCentral Hospital Affiliated to Shenyang Medical CollegeShenyangPeople’s Republic of China
  3. 3.Department of CardiologyThe First Affiliated Hospital of Jinzhou Medical UniversityJinzhouPeople’s Republic of China

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