NDLI: Characterization of the lipolytic pathways that mediate free fatty acid release during Fas/CD95-induced apoptosis

Content Provider	Springer Nature Link
Author	Iturralde, M. Pardo, J. Lacasa, E. Barrio, G. Alava, M. A. Piñeiro, A. Naval, J. Anel, A.
Copyright Year	2005
Abstract	We have undertaken a study to characterize the lipolytic pathway responsible for the generation of free fatty acids (FFA) during Fas/CD95-induced apoptosis in Jurkat cells. It was initially shown that the cellular lipid fraction that suffered the major quantitative decrease during Fas-induced apoptosis was that of phosphatidylcholine (PC). In addition, the secretion of palmitic acid-derived FFA was largely prevented by D609, an inhibitor of PC-specific phospholipase C (PC-PLC) and also by the diacylglycerol lipase (DAGL) inhibitor RHC-80267, suggesting that the secretion of these FFA during Fas-induced apoptosis is mediated by the generation of DAG by a PC-PLC activity and, sequentially, by a 1-DAGL activity which generates the FFA from its sn-1 position. The endocannabinoid 2-arachidonoyl glycerol (2-AG) should be generated as a sub-product of this pathway, but it did not accumulate inside the cells nor was secreted into the supernatant. Interestingly, the complete inhibition of free AA secretion during Fas-induced apoptosis was only achieved by using the AA trifluoromethylketone, which not only inhibits all types of phospholipase-A2 (PLA2) activities, but also the described lytic activities on 2-AG. Using a combination of RHC-80267 and the iPLA2-specific inhibitor bromoenol lactone, it was shown that the DAGL pathway also cooperates with iPLA2 in the generation of free arachidonate.
Starting Page	1369
Ending Page	1381
Page Count	13
File Format	PDF
ISSN	13608185
Journal	Apoptosis
Volume Number	10
Issue Number	6
e-ISSN	1573675X
Language	English
Publisher	Kluwer Academic Publishers
Publisher Date	2005-10-03
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	apoptosis arachidonate Fas/CD95 palmitate Cancer Research Virology Oncology Biochemistry Cell Biology
Content Type	Text
Resource Type	Article
Subject	Pharmaceutical Science Biochemistry (medical) Cell Biology Clinical Biochemistry Cancer Research Pharmacology

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