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Titolo:
Lysophosphatidylcholine induces apoptosis in AR42J cells
Autore:
Masamune, A; Sakai, Y; Satoh, A; Fujita, M; Yoshida, M; Shimosegawa, T;
Indirizzi:
Tohoku Univ, Sch Med, Dept Internal Med 3, Aoba Ku, Sendai, Miyagi 9808574, Japan Tohoku Univ Sendai Miyagi Japan 9808574 Ku, Sendai, Miyagi 9808574, Japan
Titolo Testata:
PANCREAS
fascicolo: 1, volume: 22, anno: 2001,
pagine: 75 - 83
SICI:
0885-3177(200101)22:1<75:LIAIAC>2.0.ZU;2-L
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROTEIN-KINASE-C; PLATELET-ACTIVATING-FACTOR; LYMPHOCYTE-T ACTIVATION; VEIN ENDOTHELIAL-CELLS; CULTURED HUMAN; GENE-EXPRESSION; CLUSTERIN GENE; DEATH; PHOSPHOLIPASE-A2; PANCREATITIS;
Keywords:
lysophosphatidylcholine; phospholipase A2; apoptosis; acute pancreatitis;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
45
Recensione:
Indirizzi per estratti:
Indirizzo: Masamune, A Tohoku Univ, Sch Med, Dept Internal Med 3, Aoba Ku, 1-1 SeiryoMachi, Sendai, Miyagi 9808574, Japan Tohoku Univ 1-1 Seiryo Machi Sendai Miyagi Japan 9808574 Japan
Citazione:
A. Masamune et al., "Lysophosphatidylcholine induces apoptosis in AR42J cells", PANCREAS, 22(1), 2001, pp. 75-83

Abstract

Phospholipase A2 (PLA2) has been suggested to play an important role in the pathogenesis of acute pancreatitis, in part through the PLA2-generated phospholipid by-products, most notably lysophusphatidylcholine (lyso-PC). Theeffects of lyse-PC on pancreatic acinar cells, other than the induction ofnecrosis, are poorly characterized. Here we examined the effects of lyse-PC on the induction of apoptosis in rat pancreatic AR42J cells. Lyse-PC induced apoptosis in a dose-dependent manner at 10 and 25 muM, bur induced celllysis at greater than or equal to 50 muM. Lyse-PC-induced (at 25 muM) apoptosis was not blocked by a protein kinase C inhibitor (staurosporine) or byinhibitors of caspases (acetyl-DEVD-aldehyde and benzoyloxycarbonyl-VAD-fluoromethylketone). Lyse-PC at 10 and 25 muM induced the expression of clusterin mRNA and wild-type p53. Apoptosis induction by lyse-PC (at 25 muM) wasnot inhibited by a specific antagonist of platelet-activating factor (PAF)receptor, suggesting that the action was independent of the PAF receptor. These molecular events suggest a novel role of lyse-PC in the modulation ofacinar cell function.

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Documento generato il 29/03/20 alle ore 23:48:57