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Role of tumour necrosis factor receptor-1 and nuclear factor-κB in production of TNF-α-induced pro-inflammatory microparticles in endothelial cells

Authors
 S. K. Lee  ;  S.-H. Yang  ;  I. Kwon  ;  O.-H. Lee  ;  J. H. Heo 
Citation
 THROMBOSIS AND HAEMOSTASIS, Vol.112(3) : 580-588, 2014 
Journal Title
 THROMBOSIS AND HAEMOSTASIS 
ISSN
 0340-6245 
Issue Date
2014
MeSH
Animals ; Apoptosis/genetics ; Apoptosis Regulatory Proteins/genetics ; Apoptosis Regulatory Proteins/metabolism ; Cell Adhesion/genetics ; Cell-Derived Microparticles/immunology* ; Cell-Derived Microparticles/pathology ; Cells, Cultured ; Human Umbilical Vein Endothelial Cells/immunology* ; Humans ; Inflammation Mediators/immunology* ; Intercellular Adhesion Molecule-1/genetics ; Intercellular Adhesion Molecule-1/metabolism ; Male ; Mice ; Mice, Inbred Strains ; Monocytes/physiology* ; NF-kappa B/genetics ; NF-kappa B/metabolism* ; RNA, Small Interfering/genetics ; Receptors, Tumor Necrosis Factor, Type I/genetics ; Receptors, Tumor Necrosis Factor, Type I/metabolism* ; Tumor Necrosis Factor-alpha/immunology ; Up-Regulation/genetics
Keywords
Endothelial microparticles ; NF-κB ; TNF-α ; TNFR1 ; inflammation
Abstract
Tumour necrosis factor-α (TNF-α) is upregulated in many inflammatory diseases and is also a potent agent for microparticle (MP) generation. Here, we describe an essential role of TNF-α in the production of endothelial cell-derived microparticles (EMPs) in vivo and the function of TNF-α-induced EMPs in endothelial cells. We found that TNF-α rapidly increased blood levels of EMPs in mice. Treatment of human umbilical vein endothelial cells (HUVECs) with TNF-α also induced EMP formation in a time-dependent manner. Silencing of TNF receptor (TNFR)-1 or inhibition of the nuclear factor-κB (NF-κB) in HUVECs impaired the production of TNF-α-induced EMP. Incubation of HUVECs with PKH-67-stained EMPs showed that endothelial cells readily engulfed EMPs, and the engulfed TNF-α-induced EMPs promoted the expression of pro-apoptotic molecules and upregulated intercellular adhesion molecule-1 level on the cell surface, which led to monocyte adhesion. Collectively, our findings indicate that the generation of TNF-α-induced EMPs was mediated by TNFR1 or NF-κB and that EMPs can contribute to apoptosis and inflammation of endothelial cells.
Full Text
http://th.schattauer.de/en/contents/archive/issue/1975/manuscript/21427.html
DOI
10.1160/TH13-11-0975
Appears in Collections:
1. College of Medicine (의과대학) > Research Institute (부설연구소) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Neurology (신경과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Yonsei Biomedical Research Center (연세의생명연구원) > 1. Journal Papers
1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers
Yonsei Authors
Kwon, Il(권일) ORCID logo https://orcid.org/0000-0001-9449-5646
Yang, Seung Hee(양승희)
Lee, Sung Kyul(이성결)
Lee, Ok Hee(이옥희)
Heo, Ji Hoe(허지회) ORCID logo https://orcid.org/0000-0001-9898-3321
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/99740
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