ZFIN ID: ZDB-PUB-170124-3
MicroRNA-22 regulates inflammation and angiogenesis via targeting VE-cadherin
Gu, W., Zhan, H., Zhou, X.Y., Yao, L., Yan, M., Chen, A., Liu, J., Ren, X., Zhang, X., Liu, J.X., Liu, G.
Date: 2017
Source: FEBS letters   591(3): 513-526 (Journal)
Registered Authors: Liu, Jing-xia
Keywords: VE-cadherin, endothelial inflammation, miR-22, vascular development
MeSH Terms:
  • 3' Untranslated Regions/genetics
  • Animals
  • Antigens, CD/genetics
  • Antigens, CD/metabolism*
  • Base Sequence
  • Binding Sites
  • Cadherins/genetics
  • Cadherins/metabolism*
  • Down-Regulation/genetics
  • Embryo, Nonmammalian/metabolism
  • Endothelium/pathology
  • Human Umbilical Vein Endothelial Cells/metabolism
  • Inflammation/genetics*
  • Inflammation/pathology
  • Mice
  • MicroRNAs/genetics
  • MicroRNAs/metabolism*
  • Neovascularization, Physiologic/genetics*
  • Protein Binding
  • RNA, Messenger/genetics
  • RNA, Messenger/metabolism
  • Zebrafish/embryology
  • Zebrafish/genetics*
PubMed: 28112401 Full text @ FEBS Lett.
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ABSTRACT
The vascular endothelial (VE)-cadherin functions as an endothelial barrier protein controlling endothelial permeability and leukocyte transmigration. Developmental studies indicate that VE-cadherin also plays a vital role in angiogenesis. MicroRNA-22 plays important roles in cardiovascular diseases including cardiac hypertrophy and heart failure. We identified that miR-22 interacts with VE-cadherin mRNA. Overexpression of miR-22 in endothelial cells increases the synthesis of pro-inflammatory cytokines. Injection of miR-22 results in increased myeloperoxidase activity in the mouse lungs. Moreover, miR-22 injection into the fluorescent-labeled transgenic zebrafish Tg(fli1:EGFP) embryos caused defective vascular development in the dorsal and intersegmental vessels, and vascular markers were significantly suppressed in these embryos. Our studies demonstrate that the conserved targeting of VE-cadherin by miR-22 regulates endothelial inflammation, tissue injury, and angiogenesis. This article is protected by copyright. All rights reserved.
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