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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1
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pubmed:dateCreated |
2001-1-2
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pubmed:abstractText |
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 microM, but induced cell lysis at > or = 50 microM. Lyso-PC-induced (at 25 microM) 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 microM induced the expression of clusterin mRNA and wild-type p53. Apoptosis induction by lyso-PC (at 25 microM) was not inhibited by a specific antagonist of platelet-activating factor (PAF) receptor, suggesting that the action was independent of th
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Caspases,
http://linkedlifedata.com/resource/pubmed/chemical/Clusterin,
http://linkedlifedata.com/resource/pubmed/chemical/DNA,
http://linkedlifedata.com/resource/pubmed/chemical/DNA Primers,
http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Glycoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Lysophosphatidylcholines,
http://linkedlifedata.com/resource/pubmed/chemical/Molecular Chaperones,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinase C,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Suppressor Protein p53
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0885-3177
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
22
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
75-83
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:11138976-Animals,
pubmed-meshheading:11138976-Apoptosis,
pubmed-meshheading:11138976-Blotting, Western,
pubmed-meshheading:11138976-Caspases,
pubmed-meshheading:11138976-Cell Line,
pubmed-meshheading:11138976-Clusterin,
pubmed-meshheading:11138976-DNA,
pubmed-meshheading:11138976-DNA Primers,
pubmed-meshheading:11138976-Dose-Response Relationship, Drug,
pubmed-meshheading:11138976-Enzyme Inhibitors,
pubmed-meshheading:11138976-Flow Cytometry,
pubmed-meshheading:11138976-Glycoproteins,
pubmed-meshheading:11138976-Lysophosphatidylcholines,
pubmed-meshheading:11138976-Molecular Chaperones,
pubmed-meshheading:11138976-Pancreas,
pubmed-meshheading:11138976-Protein Kinase C,
pubmed-meshheading:11138976-RNA, Messenger,
pubmed-meshheading:11138976-Rats,
pubmed-meshheading:11138976-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:11138976-Tumor Suppressor Protein p53
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pubmed:year |
2001
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pubmed:articleTitle |
Lysophosphatidylcholine induces apoptosis in AR42J cells.
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pubmed:affiliation |
Third Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Japan. amasamune@int3.med.tohoku.ac.jp
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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