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Endothelial microparticles reduce ICAM-1 expression in a microRNA-222-dependent mechanism

Endothelial microparticles (EMP) are released from activated or apoptotic endothelial cells (ECs) and can be taken up by adjacent ECs, but their effect on vascular inflammation after engulfment is largely unknown. We sought to determine the role of EMP in EC inflammation. In vitro, EMP treatment sig...

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Autores principales: Jansen, Felix, Yang, Xiaoyan, Baumann, Katharina, Przybilla, David, Schmitz, Theresa, Flender, Anna, Paul, Kathrin, Alhusseiny, Adil, Nickenig, Georg, Werner, Nikos
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley & Sons, Ltd 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4568925/
https://www.ncbi.nlm.nih.gov/pubmed/26081516
http://dx.doi.org/10.1111/jcmm.12607
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author Jansen, Felix
Yang, Xiaoyan
Baumann, Katharina
Przybilla, David
Schmitz, Theresa
Flender, Anna
Paul, Kathrin
Alhusseiny, Adil
Nickenig, Georg
Werner, Nikos
author_facet Jansen, Felix
Yang, Xiaoyan
Baumann, Katharina
Przybilla, David
Schmitz, Theresa
Flender, Anna
Paul, Kathrin
Alhusseiny, Adil
Nickenig, Georg
Werner, Nikos
author_sort Jansen, Felix
collection PubMed
description Endothelial microparticles (EMP) are released from activated or apoptotic endothelial cells (ECs) and can be taken up by adjacent ECs, but their effect on vascular inflammation after engulfment is largely unknown. We sought to determine the role of EMP in EC inflammation. In vitro, EMP treatment significantly reduced tumour necrosis factor-α-induced endothelial intercellular adhesion molecule (ICAM)-1 expression on mRNA and protein level, whereas there was no effect on vascular cell adhesion molecule-1 expression. Reduced ICAM-1 expression after EMP treatment resulted in diminished monocyte adhesion in vitro. In vivo, systemic treatment of ApoE−/− mice with EMP significantly reduced murine endothelial ICAM-1 expression. To explore the underlying mechanisms, Taqman microRNA array was performed and microRNA (miR)-222 was identified as the strongest regulated miR between EMP and ECs. Following experiments demonstrated that miR-222 was transported into recipient ECs by EMP and functionally regulated expression of its target protein ICAM-1 in vitro and in vivo. After simulating diabetic conditions, EMP derived from glucose-treated ECs contained significantly lower amounts of miR-222 and showed reduced anti-inflammatory capacity in vitro and in vivo. Finally, circulating miR-222 level was diminished in patients with coronary artery disease (CAD) compared to patients without CAD. EMPs promote anti-inflammatory effects in vitro and in vivo by reducing endothelial ICAM-1 expression via the transfer of functional miR-222 into recipient cells. In pathological hyperglycaemic conditions, EMP-mediated miR-222-dependent anti-inflammatory effects are reduced.
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spelling pubmed-45689252015-09-17 Endothelial microparticles reduce ICAM-1 expression in a microRNA-222-dependent mechanism Jansen, Felix Yang, Xiaoyan Baumann, Katharina Przybilla, David Schmitz, Theresa Flender, Anna Paul, Kathrin Alhusseiny, Adil Nickenig, Georg Werner, Nikos J Cell Mol Med Original Articles Endothelial microparticles (EMP) are released from activated or apoptotic endothelial cells (ECs) and can be taken up by adjacent ECs, but their effect on vascular inflammation after engulfment is largely unknown. We sought to determine the role of EMP in EC inflammation. In vitro, EMP treatment significantly reduced tumour necrosis factor-α-induced endothelial intercellular adhesion molecule (ICAM)-1 expression on mRNA and protein level, whereas there was no effect on vascular cell adhesion molecule-1 expression. Reduced ICAM-1 expression after EMP treatment resulted in diminished monocyte adhesion in vitro. In vivo, systemic treatment of ApoE−/− mice with EMP significantly reduced murine endothelial ICAM-1 expression. To explore the underlying mechanisms, Taqman microRNA array was performed and microRNA (miR)-222 was identified as the strongest regulated miR between EMP and ECs. Following experiments demonstrated that miR-222 was transported into recipient ECs by EMP and functionally regulated expression of its target protein ICAM-1 in vitro and in vivo. After simulating diabetic conditions, EMP derived from glucose-treated ECs contained significantly lower amounts of miR-222 and showed reduced anti-inflammatory capacity in vitro and in vivo. Finally, circulating miR-222 level was diminished in patients with coronary artery disease (CAD) compared to patients without CAD. EMPs promote anti-inflammatory effects in vitro and in vivo by reducing endothelial ICAM-1 expression via the transfer of functional miR-222 into recipient cells. In pathological hyperglycaemic conditions, EMP-mediated miR-222-dependent anti-inflammatory effects are reduced. John Wiley & Sons, Ltd 2015-09 2015-06-17 /pmc/articles/PMC4568925/ /pubmed/26081516 http://dx.doi.org/10.1111/jcmm.12607 Text en © 2015 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine. http://creativecommons.org/licenses/by/4.0/ This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Articles
Jansen, Felix
Yang, Xiaoyan
Baumann, Katharina
Przybilla, David
Schmitz, Theresa
Flender, Anna
Paul, Kathrin
Alhusseiny, Adil
Nickenig, Georg
Werner, Nikos
Endothelial microparticles reduce ICAM-1 expression in a microRNA-222-dependent mechanism
title Endothelial microparticles reduce ICAM-1 expression in a microRNA-222-dependent mechanism
title_full Endothelial microparticles reduce ICAM-1 expression in a microRNA-222-dependent mechanism
title_fullStr Endothelial microparticles reduce ICAM-1 expression in a microRNA-222-dependent mechanism
title_full_unstemmed Endothelial microparticles reduce ICAM-1 expression in a microRNA-222-dependent mechanism
title_short Endothelial microparticles reduce ICAM-1 expression in a microRNA-222-dependent mechanism
title_sort endothelial microparticles reduce icam-1 expression in a microrna-222-dependent mechanism
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4568925/
https://www.ncbi.nlm.nih.gov/pubmed/26081516
http://dx.doi.org/10.1111/jcmm.12607
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