© 2000 American Heart Association, Inc.
Vascular Biology |
Expression of Tumor Necrosis Factor-
in Cultured Human Endothelial Cells Stimulated With Lipopolysaccharide or Interleukin-1
From the Department of Pathological Physiology, Institute of Neurological Diseases (T.I., H.I., K.Fujita, K.Fujimoto, H.Y., K.S.), Department of Urology (D.K., S.K., K.M.), and Department of Dentistry and Oral Surgery (T.M.), Hirosaki University School of Medicine, Hirosaki, Japan.
Correspondence to Tadaatsu Imaizumi, MD, Department of Pathological Physiology, Institute of Neurological Diseases, Hirosaki University School of Medicine, 5 Zaifu-cho, Hirosaki 036-8562, Japan. E-mail timaizum{at}cc.hirosaki-u.ac.jp
Abstract—Tumor-necrosis
factor-
(TNF-) is a proinflammatory cytokine with a wide
variety of biological effects. The most important source of this
cytokine is monocytes/macrophages. It is a potent
agonist in the activation of endothelial cells;
however, the precise role of endothelial cells as a
source of TNF- is not known. In the present study, we addressed
the possibility that TNF- is produced by cultured human umbilical
vein endothelial cells (HUVEC) stimulated with factors
such as lipopolysaccharide (LPS) or interleukin-1 (IL-1).
LPS and IL-1 induced expression of TNF- mRNA in HUVEC. IL-1
induced expression and secretion of TNF- protein, but LPS did not
induce production of TNF- protein. Most of the TNF-
protein in cell lysate was found in the membrane fraction. The mRNA for
TNF-–converting enzyme (TACE) was expressed in unstimulated HUVEC,
and its level was not altered by treatment with LPS or IL-1.
Transfection of HUVEC with full-length cDNA encoding the precursor
TNF- enhanced secretion of TNF- protein by these cells, and
treatment of the cells with a TACE inhibitor reduced the
secretion. These results suggest that HUVEC produce TNF- and have
TACE activity. Secreted TNF- may be involved in autocrine activation
of endothelial cells, and TNF- retained in cell
membrane may serve as a juxtacrine system to activate
target cells on the endothelial surface.
Key Words: tumor necrosis factor • endothelium • lipopolysaccharide • cytokine
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