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 The role of protein kinase C in the induction of VCAM-1 expression on human umbilical vein endothelial cells

FEBS Letters ◽  
1993 ◽  
Vol 331 (3) ◽  
pp. 285-290 ◽  
Author(s):  
Theresa A. Deisher ◽  
Terri L. Haddix ◽  
Kevin F. Montgomery ◽  
Timothy H. Pohlman ◽  
Kenneth Kaushansky ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Umbilical Vein ◽  
Human Umbilical Vein ◽  
Kinase C ◽  
Umbilical Vein Endothelial Cells

scholarly journals Thioredoxin reductase is the major selenoprotein expressed in human umbilical-vein endothelial cells and is regulated by protein kinase C

1999 ◽  
Vol 342 (1) ◽  
pp. 111-117 ◽  
Author(s):  
Sue M. ANEMA ◽  
Simon W. WALKER ◽  
A. Forbes HOWIE ◽  
John R. ARTHUR ◽  
Fergus NICOL ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Umbilical Vein ◽  
Thioredoxin Reductase ◽  
Maximal Effect ◽  
Down Regulation ◽  
Human Umbilical Vein ◽  
Kinase C ◽  
Umbilical Vein Endothelial Cells

Damage to the endothelium by reactive oxygen species favours atherogenesis. Such damage can be prevented by selenium, which is thought to exert its actions through the expression of selenoproteins. The family of glutathione peroxidases (GPXs) may have antioxidant roles in the endothelium but other intracellular and extracellular selenoproteins with antioxidant actions may also be important. The selenoproteins expressed by cultured human umbilical-vein endothelial cells (HUVECs) were labelled with [75Se]selenite and separated using SDS/PAGE. HUVECs secreted no extracellular selenoproteins. There were distinct differences between the intracellular selenoprotein profile of 75Se-labelled HUVECs and those of other tissues. A single selenoprotein with a molecular mass of 58 kDa accounted for approx. 43% of the intracellular 75Se-labelled proteins in HUVECs. This protein was identified by Western blotting as the redox-active lipid-hydroperoxide-detoxifying selenoprotein, thioredoxin reductase (TR). TR expression in HUVECs was down-regulated by transiently exposing cells to the phorbol ester PMA for periods as short as 1 min. However, there was a delay of 48 h after PMA exposure before maximal down-regulation of TR was observed. The protein kinase C (PKC) inhibitor bisindolylmaleimide I hydrochloride had no effect on TR expression when added alone, but the agent prevented the down-regulation of TR expression seen with PMA. The calcium ionophore A23187 increased TR expression in HUVECs after a 12-h exposure, but the maximal effect was only observed after a 35-h exposure. These findings suggest that TR may be an important factor in the known ability of Se to protect HUVECs from peroxidative damage. Furthermore, the results also suggest that TR expression can be negatively regulated through PKC. It is possible that TR expression may be positively regulated by the calcium-signalling cascade, although TR induction by A23187 may be due to toxicity.

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