Changes of phospholipase D activity in TNF-alpha and anti-Fas/Apo1 monoclonal antibody induced apoptosis in HL-60 and A20 cells
Experimental & Molecular Medicine
; : 21-27, 1998.
Article
em En
| WPRIM
| ID: wpr-192961
Biblioteca responsável:
WPRO
ABSTRACT
The changes of phospholipase D (PLD) activity were investigated during the courses of apoptotic process induced by tumor necrosis factor (TNF)-alpha or anti-Fas/Apo1 antibody in human premyelocyte HL-60 and murine B cell lymphoma A20 cells. The treatment of recombinant TNF-alpha to HL-60 cells resulted in the increased PLD activity as determined by the phosphatidylethanol formation in the presence of 1% ethanol. The enhancement of PLD activity was also observed in the anti-Fas/Apo1 monoclonal antibody-treated A20 cells. However, the activity of PLD was maximized when HL-60 and A20 cells were treated with either TNF-alpha or anti-Fas/Apo1 monoclonal antibody for 6 h. Both TNF-alpha and anti-Fas/Apo1 monoclonal antibody increased PLD activity in a dose-dependent manner up to 200 U/ml and 200 ng/ml, respectively. When the intracellular activity of protein kinase C (PKC) was interrupted by treatment of calphostin-C, both the PLD activation and the apoptosis induced by TNF-alpha and anti-Fas/Apo1 monoclonal antibody appeared to be inhibited. Since PKC is reported to activate PLD, the results indicate that the intracellular signaling cascade via PLD may play a role in the induction of apoptosis induced by TNF-alpha and anti-Fas/Apo1 monoclonal antibody.
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Texto completo:
1
Índice:
WPRIM
Assunto principal:
Fosfolipase D
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Proteína Quinase C
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Leucemia Promielocítica Aguda
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Transdução de Sinais
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Linfoma de Células B
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Fator de Necrose Tumoral alfa
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Apoptose
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Receptores do Fator de Necrose Tumoral
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Células HL-60
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Receptor fas
Limite:
Animals
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Humans
Idioma:
En
Revista:
Experimental & Molecular Medicine
Ano de publicação:
1998
Tipo de documento:
Article