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Updated: Feb 7, 2026

Preparation and In Vitro Characterization of Magnetized miR-modified Endothelial Cells
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Preparation and In Vitro Characterization of Magnetized miR-modified Endothelial Cells

Published on: May 2, 2017

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miR-27b Suppresses Endothelial Cell Proliferation and Migration by Targeting Smad7 in Kawasaki Disease

Xing Rong1, Donghui Ge1, Danping Shen1

  • 1Children's Heart Center, the Second Affiliated Hospital and Yuying Children's Hospital, Institute of Cardiovascular Development and Translational Medicine, Wenzhou Medical University, Wenzhou, China.

Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology
|August 6, 2018
PubMed
Abstract

Insights

MicroRNA-27b (miR-27b) is elevated in Kawasaki disease (KD) and protects endothelial cells by targeting Smad7, suggesting miR-27b as a potential KD biomarker and therapeutic target.

Area of Science:

  • Molecular Biology
  • Immunology
  • Cardiovascular Research

Background:

  • MicroRNAs (miRNAs) are increasingly recognized for their roles in Kawasaki disease (KD).
  • Previous studies identified hsa-miR-27b-3p (miR-27b) as upregulated in KD serum.
  • The precise function and mechanism of miR-27b in KD pathogenesis remained unclear.

Purpose of the Study:

  • To investigate miR-27b as a potential biomarker and therapeutic target for KD.
  • To elucidate the mechanism by which miR-27b influences endothelial cell function in KD.

Main Methods:

  • Quantitative real-time PCR (qRT-PCR) to measure miR-27b and Smad7 expression.
  • Gain-of-function experiments in human umbilical vein endothelial cells (HUVECs) to assess proliferation and migration.
  • Bioinformatics analysis and luciferase reporter assays to identify and validate miR-27b targets.
  • Western blotting to analyze protein expression related to cell function and TGF-β signaling.

Main Results:

  • miR-27b was significantly upregulated in KD serum and HUVECs treated with KD serum.
  • Elevated miR-27b expression inhibited HUVEC proliferation and migration.
  • miR-27b was confirmed to target Smad7, mediating its effects on TGF-β signaling pathways in HUVECs.

Conclusions:

  • Upregulated miR-27b exhibits a protective effect on endothelial cell proliferation and migration by targeting Smad7 and modulating the TGF-β pathway.
  • miR-27b demonstrates potential as a diagnostic biomarker for KD.
  • miR-27b represents a promising therapeutic target for KD treatment.
Keywords:
BiomarkerHuman Umbilical Vein Endothelial CellKawasaki DiseaseTGF-β signaling pathwaymiR-27b

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