Tumor necrosis factor-alpha induces release of endothelial microparticles from human endothelial cells.
- Author:
Yan WANG
1
;
Jun TAO
;
Zhen YANG
;
Chang TU
;
Ming-guo XU
;
Jie-mei WANG
;
Yi-jun HUANG
Author Information
- Publication Type:Journal Article
- MeSH: Cells, Cultured; Cytoplasmic Granules; metabolism; Endothelial Cells; drug effects; metabolism; Endothelium, Vascular; cytology; Flow Cytometry; Humans; Tumor Necrosis Factor-alpha; metabolism; pharmacology; Umbilical Veins; cytology
- From: Chinese Journal of Cardiology 2005;33(12):1137-1140
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVEThe present study was designed to investigate whether Tumor necrosis factor (TNF)-alpha stimulates release of endothelial microparticles (EMPs) by human endothelial cells, and whether EMPs may serve as a promising marker for endothelial injury and dysfunction.
METHODSHuman umbilical venous endothelial cells (HUVEC) were incubated with or without TNF-alpha for 24 hours at 37 degrees C. EMPs generated on the surface of HUVEC were observed with a scanning electron microscopy. The CD31 and CD51 positive EMPs in culture supernatants were measured by flow cytometer.
RESULTSFewer vesicles were observed on cell surface of control group, in TNF-alpha-stimulated one, however, cells manifested a blebby surface (eruption phenomenon) and more vesicles on surface were observed. The levels of EMPs were significantly increased in TNF-alpha stimulated cells compared with controls [CD31 + EMP, (164 +/- 63)/1000 cells vs. (42 +/- 10)/1000 cells, P < 0.05; CD51 + EMP, (260 +/- 108)/1000 cells vs. (19 +/- 4)/1000 cells, P < 0.05].
CONCLUSIONTNF-alpha can stimulate HUVEC to release EMPs which may serve as a surrogate marker for endothelial injury and dysfunction.
