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Olof Gidlöf

Research project participant

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Extracellular Uridine Triphosphate and Adenosine Triphosphate Attenuate Endothelial Inflammation through miR-22-Mediated ICAM-1 Inhibition.

Author

  • Olof Gidlöf
  • Ramasri Sathanoori
  • Marco Magistri
  • Mohammad Ali Faghihi
  • Claes Wahlestedt
  • Björn Olde
  • David Erlinge

Summary, in English

Adenosine and uridine triphosphate (ATP and UTP) can act as extracellular signalling molecules, playing important roles in vascular biology and disease. ATP and UTP acting via the P2Y2-receptor have, for example, been shown to regulate endothelial dilatation, inflammation and angiogenesis. MicroRNAs (miRNAs), a class of regulatory, short, non-coding RNAs, have been shown to be important regulators of these biological processes. In this study, we used RNA deep-sequencing to explore changes in miRNA expression in the human microvascular endothelial cell line HMEC-1 upon UTP treatment. The expression of miR-22, which we have previously shown to target ICAM-1 mRNA in HMEC-1, increased significantly after stimulation. Up-regulation of miR-22 and down-regulation of cell surface ICAM-1 were confirmed with qRT-PCR and flow cytometry, respectively. siRNA-mediated knockdown of the P2Y2-receptor abolished the effect of UTP on miR-22 transcription. Leukocyte adhesion was significantly inhibited in HMEC-1 following miR-22 overexpression and treatment with UTP/ATP. In conclusion, extracellular UTP and ATP can attenuate ICAM-1 expression and leukocyte adhesion in endothelial cells through miR-22. © 2015 S. Karger AG, Basel.

Department/s

  • Cardiology

Publishing year

2015

Language

English

Pages

71-80

Publication/Series

Journal of Vascular Research

Volume

52

Issue

2

Document type

Journal article

Publisher

Karger

Topic

  • Cardiac and Cardiovascular Systems

Status

Published

ISBN/ISSN/Other

  • ISSN: 1423-0135