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

Sung Kyul Lee, Seung Hee Yang, Il Kwon, Ok Hee Lee, Jihoe Heo

Research output: Contribution to journalArticle

27 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)580-588
Number of pages9
JournalThrombosis and Haemostasis
Issue number3
Publication statusPublished - 2014 Jan 1


All Science Journal Classification (ASJC) codes

  • Hematology

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