scholarly journals Post-transcriptional regulation of interleukin 1 alpha in various strains of young and senescent human umbilical vein endothelial cells.

1994 ◽  
Vol 91 (4) ◽  
pp. 1559-1563 ◽  
Author(s):  
S. Garfinkel ◽  
S. Brown ◽  
J. H. Wessendorf ◽  
T. Maciag
Keyword(s):  
Endothelial Cells ◽  
Transcriptional Regulation ◽  
Umbilical Vein ◽  
Interleukin 1 ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells ◽  
Post Transcriptional Regulation

scholarly journals Interleukin-1 Enhances the Ability of Cultured Human Umbilical Vein Endothelial Cells to Oxidize Linoleic Acid

1995 ◽  
Vol 270 (29) ◽  
pp. 17279-17286 ◽  
Author(s):  
Mercedes Camacho ◽  
Nuria Godessart ◽  
Rosa Antón ◽  
Montserrat Garca ◽  
Lus Vila
Keyword(s):  
Endothelial Cells ◽  
Linoleic Acid ◽  
Umbilical Vein ◽  
Interleukin 1 ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

Induction of Tissue Factor Synthesis in Human Umbilical Vein Endothelial Cells Involves Protein Kinase C

1992 ◽  
Vol 67 (04) ◽  
pp. 473-477 ◽  
Author(s):  
Kjell Sverre Pettersen ◽  
Merete Thune Wiiger ◽  
Nobuhiro Narahara ◽  
Kiyoshi Andoh ◽  
Gustav Gaudernack ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Tissue Factor ◽  
Umbilical Vein ◽  
Interleukin 1 ◽  
Interleukin 1Β ◽  
Human Umbilical Vein ◽  
Kinase C ◽  
Umbilical Vein Endothelial Cells

SummaryIncubation of human umbilical vein endothelial cells with one of the following compounds: endotoxin, recombinant interleukin-1β, recombinant tumor necrosis factor α, allogenic lymphocyte subpopulations or phorbol ester resulted in significant induction of tissue factor synthesis. Diacylglycerol had the same effect and also enhanced synergistically the induction caused by endotoxin and interleukin-1β. Two different inhibitors of protein kinase C, H7 and sphingosine, inhibited tissue factor synthesis at concentrations which did not depress protein synthesis in general, suggesting that protein kinase C is involved in the processes leading to tissue factor synthesis. Cells down-regulated for the tissue factor response to TPA responded essentially normally to endotoxin and interleukin-1 with regard to tissue factor synthesis.

scholarly journals Induction of interleukin-1 and subsequent tissue factor expression by anti-proteinase 3 antibodies in human umbilical vein endothelial cells

1997 ◽  
Vol 40 (11) ◽  
pp. 2030-2038 ◽  
Author(s):  
Michel de Bandt ◽  
Véronique Ollivier ◽  
Catherine Babin-Chevaye ◽  
Fouzi Khechaï ◽  
Dominique de Prost ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Tissue Factor ◽  
Umbilical Vein ◽  
Interleukin 1 ◽  
Proteinase 3 ◽  
Tissue Factor Expression ◽  
Human Umbilical Vein ◽  
Factor Expression ◽  
Umbilical Vein Endothelial Cells

Alteration in glycosaminoglycan metabolism and surface charge on human umbilical vein endothelial cells induced by cytokines, endotoxin and neutrophils

1992 ◽  
Vol 102 (4) ◽  
pp. 821-832 ◽  
Author(s):  
N.J. Klein ◽  
G.I. Shennan ◽  
R.S. Heyderman ◽  
M. Levin
Keyword(s):  
Endothelial Cells ◽  
Umbilical Vein ◽  
Interleukin 1 ◽  
Cellular Interactions ◽  
Anionic Sites ◽  
Human Umbilical Vein ◽  
Inflammatory Stimuli ◽  
Concomitant Reduction ◽  
Glycosaminoglycan Metabolism ◽  
Umbilical Vein Endothelial Cells

There is increasing evidence that the glycosaminoglycan (GAG) component of the vascular endothelium is important in regulating vascular permeability, thromboresistance and cellular interactions. We have investigated the GAG metabolism of cultured human umbilical vein endothelial cells (HUVEC) in response to a range of inflammatory stimuli. Using both chemical measurement of cellular and supernatant GAGS and 35S labelling to identify newly synthesised GAGS, interleukin 1 (IL1), tumour necrosis factor (TNF) and interferon gamma (IFN gamma) were shown to influence sulphated GAG metabolism significantly. IL1 and TNF caused a marked increase in culture supernatant GAGS and a concomitant reduction in cell-associated GAGS. This was shown histochemically to be associated with a marked reduction and redistribution of endothelial surface anionic sites. The addition of neutrophils to HUVEC pretreated with Escherichia coli endotoxin, IL1 or TNF resulted in a further reduction in both cellular GAGS and surface anionic sites. These results suggest that changes in endothelial cell GAG metabolism during inflammation may contribute to the disturbance of vascular endothelial homeostasis associated with infectious and inflammatory states.

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