Reference : Endothelin-1 does not modulate O2.release and [Ca(2+)]i variations in resting or diff...
Scientific journals : Article
Life sciences : Biochemistry, biophysics & molecular biology
http://hdl.handle.net/10993/5729
Endothelin-1 does not modulate O2.release and [Ca(2+)]i variations in resting or differentiated HL-60 cells
English
Gallois, A. [> >]
Bueb, Jean-Luc mailto [University of Luxembourg > Faculty of Science, Technology and Communication (FSTC) > Life Science Research Unit >]
Tschirhart, Eric mailto [University of Luxembourg > Faculty of Science, Technology and Communication (FSTC) > Life Science Research Unit >]
1996
Fundamental & Clinical Pharmacology
Blackwell Science
10
1
28-32
Yes (verified by ORBilu)
0767-3981
1472-8206
Oxford
United Kingdom
[en] drug effects ; Dose-Response Relationship, Drug ; Endothelins ; Fura-2 ; HL-60 Cells ; Humans ; N-Formylmethionine Leucyl-Phenylalanine ; Neutrophils ; Superoxides ; metabolism ; pharmacology ; Calcium
[en] Endothelin-1 (ET-1) by itself was not an effective stimulus for inducing superoxide (O2.) generation in human resting or DMSO-differentiated neutrophil-like HL-60 cells. ET-1 (0.01-100 nM) was not able to modulate O2. generation stimulated by the chemotactic peptide N-formyl-L-methionyl-L-leucyl-L-phenylalanine (fMLP, EC50 = 4.24 +/- 1.63 nM in the absence and 3.16 +/- 1.95 nM in the presence of ET-1). Neither did ET-1 (0.01-100 nM) promote the mobilization of intracellular calcium ions or modulate fMLP-induced [Ca(2+)]i increase in this model of human neutrophils. Phosphoramidon, a neutral endopeptidase inhibitor, was not able to reveal any biological (O2.) or biochemical ([Ca(2+)]i response to ET-1 in the absence or in the presence of fMLP in these cells. These results indicate that DMSO-differentiated neutrophil-like HL-60 cells are not sensitive to ET-1 in terms of O2. generation or [Ca(2+)]i variations.
http://hdl.handle.net/10993/5729

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