Inhibition of Human Complement-Dependent Cell Lysis by Bovine Aortic Endothelial Cells Transfected with Membrane-Bound Complement-Regulatory Factor (DAF and HRF20) Gene Using a Retroviral Vector

1996 ◽  
Vol 28 (6) ◽  
pp. 440-446 ◽  
Author(s):  
S. Hayashi ◽  
K. Isobe ◽  
N. Emi ◽  
I. Yokoyama ◽  
H. Okada ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Lysis ◽  
Retroviral Vector ◽  
Human Complement ◽  
Regulatory Factor ◽  
Aortic Endothelial Cells ◽  
Bovine Aortic Endothelial Cells ◽  
Dependent Cell ◽  
Membrane Bound ◽  
Aortic Endothelial

scholarly journals Palytoxin-induced cell death cascade in bovine aortic endothelial cells

2006 ◽  
Vol 291 (4) ◽  
pp. C657-C667 ◽  
Author(s):  
William P. Schilling ◽  
Deborah Snyder ◽  
William G. Sinkins ◽  
Mark Estacion
Keyword(s):  
Endothelial Cells ◽  
Cell Death ◽  
Fluorescent Protein ◽  
Time Lapse ◽  
Cell Lysis ◽  
Monovalent Cation ◽  
Aortic Endothelial Cells ◽  
Bovine Aortic Endothelial Cells ◽  
Cell Death Cascade ◽  
Aortic Endothelial

The plasmalemmal Na+-K+-ATPase (NKA) pump is the receptor for the potent marine toxin palytoxin (PTX). PTX binds to the NKA and converts the pump into a monovalent cation channel that exhibits a slight permeability to Ca2+. However, the ability of PTX to directly increase cytosolic free Ca2+ concentration ([Ca2+]i) via Na+ pump channels and to initiate Ca2+ overload-induced oncotic cell death has not been examined. Thus the purpose of this study was to determine the effect of PTX on [Ca2+]i and the downstream events associated with cell death in bovine aortic endothelial cells. PTX (3–100 nM) produced a graded increase in [Ca2+]i that was dependent on extracellular Ca2+. The increase in [Ca2+]i initiated by 100 nM PTX was blocked by pretreatment with ouabain with an IC50 < 1 μM. The elevation in [Ca2+]i could be reversed by addition of ouabain at various times after PTX, but this required much higher concentrations of ouabain (0.5 mM). These results suggest that the PTX-induced rise in [Ca2+]i occurs via the Na+ pump. Subsequent to the rise in [Ca2+]i, PTX also caused a concentration-dependent increase in uptake of the vital dye ethidium bromide (EB) but not YO-PRO-1. EB uptake was also blocked by ouabain added either before or after PTX. Time-lapse video microscopy showed that PTX ultimately caused cell lysis as indicated by release of transiently expressed green fluorescent protein (molecular mass 27 kDa) and rapid uptake of propidium iodide. Cell lysis was 1) greatly delayed by removing extracellular Ca2+ or by adding ouabain after PTX, 2) blocked by the cytoprotective amino acid glycine, and 3) accompanied by dramatic membrane blebbing. These results demonstrate that PTX initiates a cell death cascade characteristic of Ca2+ overload.

Effects of Dipyrone on Prostaglandin Production by Human Platelets and Cultured Bovine Aortic Endothelial Cells

1983 ◽  
Vol 49 (02) ◽  
pp. 132-137 ◽  
Author(s):  
A Eldor ◽  
G Polliack ◽  
I Vlodavsky ◽  
M Levy
Keyword(s):  
Endothelial Cells ◽  
Arachidonic Acid ◽  
Competitive Inhibition ◽  
Inhibitory Effect ◽  
Human Platelets ◽  
Ionophore A23187 ◽  
Aortic Endothelial Cells ◽  
Bovine Aortic Endothelial Cells ◽  
Aortic Endothelial

SummaryDipyrone and its metabolites 4-methylaminoantipyrine, 4-aminoantipyrine, 4-acetylaminoantipyrine and 4-formylaminoan- tipyrine inhibited the formation of thromboxane A2 (TXA2) during in vitro platelet aggregation induced by ADP, epinephrine, collagen, ionophore A23187 and arachidonic acid. Inhibition occurred after a short incubation (30–40 sec) and depended on the concentration of the drug or its metabolites and the aggregating agents. The minimal inhibitory concentration of dipyrone needed to completely block aggregation varied between individual donors, and related directly to the inherent capacity of their platelets to synthesize TXA2.Incubation of dipyrone with cultured bovine aortic endothelial cells resulted in a time and dose dependent inhibition of the release of prostacyclin (PGI2) into the culture medium. However, inhibition was abolished when the drug was removed from the culture, or when the cells were stimulated to produce PGI2 with either arachidonic acid or ionophore A23187.These results indicate that dipyrone exerts its inhibitory effect on prostaglandins synthesis by platelets or endothelial cells through a competitive inhibition of the cyclooxygenase system.

scholarly journals Ethanolamine metabolism in cultured bovine aortic endothelial cells.

1990 ◽  
Vol 265 (13) ◽  
pp. 7195-7201
Author(s):  
B A Lipton ◽  
E P Davidson ◽  
B H Ginsberg ◽  
M A Yorek
Keyword(s):  
Endothelial Cells ◽  
Aortic Endothelial Cells ◽  
Bovine Aortic Endothelial Cells ◽  
Aortic Endothelial

Microcarrier cultivation of bovine aortic endothelial cells in spinner vessels and a membrane stirred bioreactor

1996 ◽  
Vol 18 (3) ◽  
pp. 193-206 ◽  
Author(s):  
Johannes M�thing ◽  
Sevim Duvar ◽  
Susann Nerger ◽  
Heino B�ntemeyer ◽  
J�rgen Lehmann
Keyword(s):  
Endothelial Cells ◽  
Aortic Endothelial Cells ◽  
Stirred Bioreactor ◽  
Bovine Aortic Endothelial Cells ◽  
Aortic Endothelial
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