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Article

CTBP1‑AS2 inhibits proliferation and induces autophagy in ox‑LDL‑stimulated vascular smooth muscle cells by regulating miR‑195‑5p/ATG14

  • Authors:
    • Yang Wang
    • Cheng‑Xin Zhang
    • Sheng‑Lin Ge
    • Wen‑Hui Gong
  • View Affiliations / Copyright

    Affiliations: Department of Cardiovascular Surgery, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230022, P.R. China
  • Pages: 839-848
    |
    Published online on: June 2, 2020
       https://doi.org/10.3892/ijmm.2020.4624
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Abstract

Atherosclerosis (AS) is a chronic progressive disease caused by injury and functional changes in vascular smooth muscle cells (VSMCs). Long non‑coding RNAs (lncRNAs) are pivotal regulators in AS development. The present study aimed to explore the roles and molecular mechanisms of lncRNA CTBP1‑AS2 in AS progression. A dual‑luciferase reporter assay confirmed that miR‑195‑5p is a downstream target miRNA of lncRNA CTBP1‑AS2 and miR‑195‑5p was increased in AS. The expression levels of miR‑195‑5p and CTBP1‑AS2 in the serums of patients with AS and human aorta vascular smooth muscle cells was increased or decreased, respectively, following treatment with oxidized low‑density lipoprotein (ox‑LDL). Functional experiments showed that the overexpression of lncRNA CTBP1‑AS2 inhibited the proliferation of HA‑VSMCs and promoted their autophagy following ox‑LDL treatment. This effect could be reversed by treatment with ROC‑325, the inhibitor of autophagy, or miR‑195‑5p mimics. Autophagy related 14 (ATG14) was identified to be a target of miR‑195‑5p, and lncRNA CTBP1‑AS2 promoted ATG14 expression by serving as a competing endogenous RNA of miR‑195‑5p. The present study revealed that lncRNA CTBP1‑AS2 may serve a role in AS by inhibiting the proliferation and promoting the autophagy of VSMCs through ATG14 modulation via miR‑195‑5p. These data may provide a novel therapeutic target for AS.
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Copy and paste a formatted citation
Spandidos Publications style
Wang Y, Zhang CX, Ge SL and Gong WH: CTBP1‑AS2 inhibits proliferation and induces autophagy in ox‑LDL‑stimulated vascular smooth muscle cells by regulating miR‑195‑5p/ATG14. Int J Mol Med 46: 839-848, 2020.
APA
Wang, Y., Zhang, C., Ge, S., & Gong, W. (2020). CTBP1‑AS2 inhibits proliferation and induces autophagy in ox‑LDL‑stimulated vascular smooth muscle cells by regulating miR‑195‑5p/ATG14. International Journal of Molecular Medicine, 46, 839-848. https://doi.org/10.3892/ijmm.2020.4624
MLA
Wang, Y., Zhang, C., Ge, S., Gong, W."CTBP1‑AS2 inhibits proliferation and induces autophagy in ox‑LDL‑stimulated vascular smooth muscle cells by regulating miR‑195‑5p/ATG14". International Journal of Molecular Medicine 46.2 (2020): 839-848.
Chicago
Wang, Y., Zhang, C., Ge, S., Gong, W."CTBP1‑AS2 inhibits proliferation and induces autophagy in ox‑LDL‑stimulated vascular smooth muscle cells by regulating miR‑195‑5p/ATG14". International Journal of Molecular Medicine 46, no. 2 (2020): 839-848. https://doi.org/10.3892/ijmm.2020.4624
Copy and paste a formatted citation
x
Spandidos Publications style
Wang Y, Zhang CX, Ge SL and Gong WH: CTBP1‑AS2 inhibits proliferation and induces autophagy in ox‑LDL‑stimulated vascular smooth muscle cells by regulating miR‑195‑5p/ATG14. Int J Mol Med 46: 839-848, 2020.
APA
Wang, Y., Zhang, C., Ge, S., & Gong, W. (2020). CTBP1‑AS2 inhibits proliferation and induces autophagy in ox‑LDL‑stimulated vascular smooth muscle cells by regulating miR‑195‑5p/ATG14. International Journal of Molecular Medicine, 46, 839-848. https://doi.org/10.3892/ijmm.2020.4624
MLA
Wang, Y., Zhang, C., Ge, S., Gong, W."CTBP1‑AS2 inhibits proliferation and induces autophagy in ox‑LDL‑stimulated vascular smooth muscle cells by regulating miR‑195‑5p/ATG14". International Journal of Molecular Medicine 46.2 (2020): 839-848.
Chicago
Wang, Y., Zhang, C., Ge, S., Gong, W."CTBP1‑AS2 inhibits proliferation and induces autophagy in ox‑LDL‑stimulated vascular smooth muscle cells by regulating miR‑195‑5p/ATG14". International Journal of Molecular Medicine 46, no. 2 (2020): 839-848. https://doi.org/10.3892/ijmm.2020.4624
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