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MiR-506-3p Promotes the Proliferation and Migration of Vascular Smooth Muscle Cells via Targeting KLF4.

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  • Author(s): Dong H;Dong H;Dong H; Jiang G; Jiang G; Zhang J; Zhang J; Kang Y; Kang Y
  • Source:
    Pathobiology : journal of immunopathology, molecular and cellular biology [Pathobiology] 2021; Vol. 88 (4), pp. 277-288. Date of Electronic Publication: 2021 Apr 21.
  • Publication Type:
    Journal Article
  • Language:
    English
  • Additional Information
    • Source:
      Publisher: S. Karger Country of Publication: Switzerland NLM ID: 9007504 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1423-0291 (Electronic) Linking ISSN: 10152008 NLM ISO Abbreviation: Pathobiology Subsets: MEDLINE
    • Publication Information:
      Original Publication: Basel ; New York : S. Karger, c1990-
    • Subject Terms:
      Atherosclerosis/*pathology ; Cell Movement/*genetics ; Kruppel-Like Transcription Factors/*genetics ; MicroRNAs/*genetics ; Myocytes, Smooth Muscle/*physiology; Animals ; Apolipoproteins E/genetics ; Cell Proliferation ; Cells, Cultured ; Humans ; Kruppel-Like Factor 4 ; Lipoproteins, LDL/pharmacology ; Mice ; Mice, Inbred C57BL ; Muscle, Smooth, Vascular/cytology ; Myocytes, Smooth Muscle/drug effects ; Signal Transduction
    • Abstract:
      Background: The dysregulation of proliferation and migration of vascular smooth muscle cells (VSMCs) is one of the major causes of atherosclerosis (AS). Accumulating studies confirm that Kruppel-like factor 4 (KLF4) can regulate the proliferation and differentiation of VSMCs through multiple signaling pathways. However, the mechanism of KLF4 dysregulation remains unknown.
      Methods: Apolipoprotein E-knockout (ApoE-/-) mice and human VSMCs were used to establish AS animal model and cell model, respectively. qRT-PCR was employed to determine the expressions of miR-506-3p and KLF4. Cell Counting Kit -8, Transwell, TUNEL assays, and flow cytometry were performed to measure the proliferation, migration, and apoptosis of VSMCs. The upstream miRNAs of KLF4 were predicted by microT, miRanda, miRmap, and TargetScan databases. The interaction between KLF4 and miR-506-3p was confirmed using qRT-PCR, Western blot, and luciferase reporter gene assay.
      Results: KLF4 expression was significantly decreased in the VSMCs of ApoE-/- mice fed with high-fat diet and in human VSMCs treated with oxidized low-density lipoprotein in time-dependent and dose-dependent manners. The transfection of miR-506-3p mimics or KLF4 shRNA promoted the proliferation and migration of VSMCs but inhibited the apoptosis while miR-506-3p inhibitors and pcDNA3.1-KLF4 exerted opposite effects. Additionally, KLF4 was confirmed as a target gene of miR-506-3p and could be negatively regulated by miR-506-3p.
      Conclusion: MiR-506-3p can promote the proliferation and migration of VSMCs via targeting KLF4, which can probably contribute to the pathogenesis of AS.
      (© 2021 S. Karger AG, Basel.)
    • Contributed Indexing:
      Keywords: Atherosclerosis; Kruppel-like transcription factor 4; Vascular smooth muscle cell; miR-506-3p
    • Accession Number:
      0 (Apolipoproteins E)
      0 (KLF4 protein, human)
      0 (Klf4 protein, mouse)
      0 (Kruppel-Like Factor 4)
      0 (Kruppel-Like Transcription Factors)
      0 (Lipoproteins, LDL)
      0 (MIRN506 microRNA, human)
      0 (MicroRNAs)
      0 (oxidized low density lipoprotein)
    • Publication Date:
      Date Created: 20210421 Date Completed: 20211111 Latest Revision: 20211204
    • Publication Date:
      20250114
    • Accession Number:
      10.1159/000513506
    • Accession Number:
      33882484