Lysophosphatidylcholine induces apoptosis in AR42J cells

Atsushi Masamune, Yoshitaka Sakai, Akihiko Satoh, Motokazu Fujita, Masayoshi Yoshida, Tooru Shimosegawa

Research output: Contribution to journalArticlepeer-review

52 Citations (Scopus)


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 lysophosphatidylcholine (lyso-PC). The effects of lyso-PC on pancreatic acinar cells, other than the induction of necrosis, are poorly characterized. Here we examined the effects of lyso-PC on the induction of apoptosis in rat pancreatic AR42J cells. Lyso-PC induced apoptosis in a dose-dependent manner at 10 and 25 μM, but induced cell lysis at ≥50 μM. Lyso-PC-induced (at 25 μM) apoptosis was not blocked by a protein kinase C inhibitor (staurosporine) or by inhibitors of caspases (acetyl-DEVD-aldehyde and benzoyloxycarbonyl-VAD-fluoromethylketone). Lyso-PC at 10 and 25 μM induced the expression of clusterin mRNA and wild-type p53. Apoptosis induction by lyso-PC (at 25 μM) was not 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 lyso-PC in the modulation of acinar cell function.

Original languageEnglish
Pages (from-to)75-83
Number of pages9
Issue number1
Publication statusPublished - 2001


  • Acute pancreatitis
  • Apoptosis
  • Lysophosphatidylcholine
  • Phospholipase A2

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism
  • Hepatology
  • Endocrinology


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