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A more recent version of this article appeared on June 1, 2005

Papers In Press, published online ahead of print March 16, 2005
J. Lipid Res., doi:10.1194/jlr.M400516-JLR200
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Submitted on December 27, 2004
Revised on February 28, 2005
Accepted on March 3, 2005

Alpha-linolenic acid-containing GM1a induces apoptosis in Neuro2a cells: application of SCDase for remodeling of fatty acids of glycosphingolipids

Tetsuto Nakagawa, Akio Morotomi, Motohiro Tani, Noriyuki Sueyoshi, Hironobu Komori, and Makoto Ito

Department of Bioscience and Biotechnology, Kyushu University, Fukuoka, Fukuoka 812-8581

Corresponding Author: makotoi{at}agr.kyushu-u.ac.jp

GM1a, a major ganglioside of nerve tissues, is known to support and protect neuronal functions while lyso-GM1a induces apoptosis inneuronal cells (J. Lipid Res. 2001. 42: 1197-1202). Here, we report that Alpha-linolenic acid-containing GM1a (C18:3-GM1a) induced apoptosis in adifferent manner from lyso-GM1a. Intranucleosomal DNA fragmentation, chromatin condensation, and caspase activation, alltypical features of apoptosis, were observed when mouse neuroblastoma Neuro2a cells were cultured with C18:3-GM1a but notGM1a containing stearic acid (C18:0) or oleic acid (C18:1). The phenotype of Neuro2a cells induced by C18:3-GM1a was similar to thatevoked by lyso-GM1a. However, lyso-GM1a caused a complete disruption of lipid microdomains of Neuro2a cells and hemolysis ofsheep erythrocytes while C18:3-GM1a did neither. C18:3-GM1a, but not lyso-GM1a, was found to be abundant in lipid microdomains after theremoval of loosely bound GM1a by bovine serum albumin. The activation of SAPK/JNK in Neuro2a cells was observed with lyso-GM1abut not C18:3-GM1a. These results indicate that the mechanism of apoptosis induced by C18:3-GM1a is distinct from that caused by lyso-GM1a. This study also clearly shows that fatty acid composition of gangliosides significantly affected their pharmacological activities whenadded to the cell cultures.


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