Open Access

Upregulation of miR‑423 improves autologous vein graft restenosis via targeting ADAMTS‑7

  • Authors:
    • Wenjun Ren
    • Liwen Liang
    • Yongwu Li
    • Fei‑Yu Wei
    • Ninghui Mu
    • Libin Zhang
    • Wei He
    • Yu Cao
    • Da Xiong
    • Hongrong Li
  • View Affiliations

  • Published online on: December 5, 2019     https://doi.org/10.3892/ijmm.2019.4419
  • Pages: 532-542
  • Copyright: © Ren et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Coronary artery bypass graft (CABG) is one of the primary methods of treating coronary heart disease (CHD); however, vein graft restenosis is a major limiting factor of the effectiveness of CABG. Emerging evidence has indicated that miR‑423 is associated with vascular diseases. Additionally, upregulation of a disintegrin and metalloproteinase with thrombospondin motifs‑7 (ADAMTS‑7) contributes to neointima formation by promoting the proliferation and migration of vascular smooth muscle cells and inhibiting the proliferation and migration of endothelial cells. The aim of the present study was to examine the effects of miR‑423 target, ADAMTS‑7, on regulating vein graft disease and identify novel biomarkers for use in therapy of vein graft failure (VGF). Aberrant expression of miR‑423 in plasma of patients with CHD prior to and following CABG confirms that miR‑423 may be a suitable target for preventing VGF. Furthermore, a dual‑luciferase reporter gene assay indicated that miR‑423 directly interacted with ADAMTS‑7 and suppressed its expression. Ectopic expression of miR‑423 suppressed ADAMTS‑7, resulting in decreased proliferation and migration rates of human umbilical vein smooth muscle cells by targeting ADAMTS‑7, but resulted in increased proliferation and migration of human umbilical vein endothelial cells in vitro. Overexpression of miR‑423 also enhanced re‑endothelialization and decreased neointimal formation in a rat vein graft model. In conclusion, the results of the present study demonstrated that the miR‑423/ADAMTS‑7 axis may possess potential clinical value for the prevention and treatment of restenosis in patients with CHD following CABG.
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February-2020
Volume 45 Issue 2

Print ISSN: 1107-3756
Online ISSN:1791-244X

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Copy and paste a formatted citation
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Spandidos Publications style
Ren W, Liang L, Li Y, Wei FY, Mu N, Zhang L, He W, Cao Y, Xiong D, Li H, Li H, et al: Upregulation of miR‑423 improves autologous vein graft restenosis via targeting ADAMTS‑7 . Int J Mol Med 45: 532-542, 2020.
APA
Ren, W., Liang, L., Li, Y., Wei, F., Mu, N., Zhang, L. ... Li, H. (2020). Upregulation of miR‑423 improves autologous vein graft restenosis via targeting ADAMTS‑7 . International Journal of Molecular Medicine, 45, 532-542. https://doi.org/10.3892/ijmm.2019.4419
MLA
Ren, W., Liang, L., Li, Y., Wei, F., Mu, N., Zhang, L., He, W., Cao, Y., Xiong, D., Li, H."Upregulation of miR‑423 improves autologous vein graft restenosis via targeting ADAMTS‑7 ". International Journal of Molecular Medicine 45.2 (2020): 532-542.
Chicago
Ren, W., Liang, L., Li, Y., Wei, F., Mu, N., Zhang, L., He, W., Cao, Y., Xiong, D., Li, H."Upregulation of miR‑423 improves autologous vein graft restenosis via targeting ADAMTS‑7 ". International Journal of Molecular Medicine 45, no. 2 (2020): 532-542. https://doi.org/10.3892/ijmm.2019.4419