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miRNA-27b modulates endothelial cell angiogenesis by directly targeting Naa15 in atherogenesis. | LitMetric

miRNA-27b modulates endothelial cell angiogenesis by directly targeting Naa15 in atherogenesis.

Atherosclerosis

The State Key Laboratory of Medical Genomics, Shanghai Key Laboratory of Hypertension, Ruijin Hospital, Shanghai Institute of Hypertension, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China; Key Laboratory of Stem Cell Biology and Laboratory of Vascular Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China. Electronic address:

Published: November 2016

AI Article Synopsis

  • * Researchers used CCR6ApoE-/- mice on a high-fat diet to evaluate the impact of CCR6 deficiency on plaque size and inflammatory markers, finding a significant reduction in plaque development and related cellular responses.
  • * The findings suggest that deleting CCR6 can slow atherosclerosis by decreasing macrophage accumulation and CCL20 secretion, with miRNA-27b playing a key role in regulating the CCL20/CCR6 axis by targeting the gene Naa15.

Article Abstract

Background And Aims: The CCL20/CCR6 axis has been shown to play a vital role in the pathogenesis of atherosclerosis (AS). However, the regulatory mechanism remains unclear. Here, we studied the miRNA-mediated epigenetic regulation of the CCL20/CCR6 axis in atherogenesis.

Methods: CCR6ApoE-/- and CCR6ApoE-/- mice were fed a high-fat diet for 24 weeks. Plaque size was evaluated via ultrasound biomicroscope and hematoxylin and eosin. Protein expression were measured by Western blotting or immunofluorescence/immunohistochemistry or ELISA, and gene mRNA levels were detected by RT-PCR. Seven hundred and sixty miRNAs were screened via miRNA profiling. miRNA-27b target genes were predicted using software and verified with a dual luciferase reporter assay. The tube formation of mouse aortic endothelial cells (MAECs) was performed on Matrigel.

Results: In contrast to wild-type ApoE-/- mice, CCR6 deficiency led to a significantly decreased plaque size, CD31, CCR6, CCL20 expression and number of CCL20 macrophages in atherosclerotic plaques. Stimulation of mouse primary peritoneal macrophages (MPPMs) resulted in increased IL-23 release. miRNA-27b was the most highly expressed (5.19-fold increase) miRNA among the 760 miRNAs screened in the vessel. Naa15 was verified as miRNA-27b target gene, which was diminished in the plaques. Transfection of siRNA Naa15 or miRNA-27b mimic into MAECs caused an increase tube formation.

Conclusions: CCR6 deletion effectively ameliorates atherosclerosis progression by reducing macrophage accumulation, resulting in reduced secretion of CCL20 and IL-23. Mechanistically, the decreased miRNA-27b regulates the activity of the CCL20/CCR6 axis by targeting Naa15, and promotes plaque stability in atherosclerosis.

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Source
http://dx.doi.org/10.1016/j.atherosclerosis.2016.10.007DOI Listing

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