HDL-transferred microRNA-223 regulates ICAM-1 expression in endothelial cells

Fatiha Tabet (), Kasey C. Vickers, Luisa F. Cuesta Torres, Carrie B. Wiese, Bassem M. Shoucri, Gilles Lambert, Claire Catherinet, Leonel Prado-Lourenco, Michael G. Levin, Seth Thacker, Praveen Sethupathy, Philip J. Barter, Alan T. Remaley and Kerry-Anne Rye
Additional contact information
Fatiha Tabet: Centre for Vascular Research, The University of New South Wales
Kasey C. Vickers: National Heart, Lung and Blood Institute, National Institutes of Health
Luisa F. Cuesta Torres: Centre for Vascular Research, The University of New South Wales
Carrie B. Wiese: Vanderbilt University School of Medicine
Bassem M. Shoucri: National Heart, Lung and Blood Institute, National Institutes of Health
Gilles Lambert: Université de Nantes, Faculté de Médecine, Laboratoire Inserm U957
Claire Catherinet: Lipid Research Group, The Heart Research Institute
Leonel Prado-Lourenco: Centre for Vascular Research, The University of New South Wales
Michael G. Levin: National Heart, Lung and Blood Institute, National Institutes of Health
Seth Thacker: National Heart, Lung and Blood Institute, National Institutes of Health
Praveen Sethupathy: University of North Carolina
Philip J. Barter: Centre for Vascular Research, The University of New South Wales
Alan T. Remaley: National Heart, Lung and Blood Institute, National Institutes of Health
Kerry-Anne Rye: Centre for Vascular Research, The University of New South Wales

Nature Communications, 2014, vol. 5, issue 1, 1-14

Abstract: Abstract High-density lipoproteins (HDL) have many biological functions, including reducing endothelial activation and adhesion molecule expression. We recently reported that HDL transport and deliver functional microRNAs (miRNA). Here we show that HDL suppresses expression of intercellular adhesion molecule 1 (ICAM-1) through the transfer of miR-223 to endothelial cells. After incubation of endothelial cells with HDL, mature miR-223 levels are significantly increased in endothelial cells and decreased on HDL. However, miR-223 is not transcribed in endothelial cells and is not increased in cells treated with HDL from miR-223−/− mice. HDL inhibit ICAM-1 protein levels, but not in cells pretreated with miR-223 inhibitors. ICAM-1 is a direct target of HDL-transferred miR-223 and this is the first example of an extracellular miRNA regulating gene expression in cells where it is not transcribed. Collectively, we demonstrate that HDL’s anti-inflammatory properties are conferred, in part, through HDL-miR-223 delivery and translational repression of ICAM-1 in endothelial cells.

Date: 2014
References: Add references at CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/ncomms4292 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms4292

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/ncomms4292

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().