Taipei Medical University

A B C D E F G H I J K L M N O P Q R S T U V W X Y Z
Yang DI
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------>journal_name=Neurobiol Dis
------>paper_name=Neutral sphingomyelinase activation in endothelial and glial cell death induced by amyloid beta-peptide.
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------>fullAbstract=We have explored the molecular mechanism underlying amyloid beta-peptide (Abeta)-mediated cytotoxicity in vitro. Exposure of murine cerebral endothelial cells (CECs) or C6 glioma cells to Abeta25-35 resulted in dose-dependent cell death. Ceramide is a pro-apoptotic lipid mediator. Forced elevation of cellular ceramide levels, either by application of an exogenous C2 ceramide analogue or bacterial sphingomyelinase that induces endogenous ceramide release from sphingomyelin, mimicked Abeta25-35 cytotoxicity in both CECs and C6 glioma cells. Abeta25-35-induced synthesis of ceramide was selectively mediated by activation of neutral sphingomyelinase (nSMase), but not acidic sphingomyelinase (aSMase) or ceramide synthase. Both 3-O-Me-SM and N-acetyl-L-cysteine, the selective and nonselective pharmacological inhibitors of nSMase, respectively, suppressed nSMase activation, ceramide production, and cytotoxic action induced by Abeta25-35 in CECs. Furthermore, genetic knockdown of nSMase by an antisense strategy rendered C6 glioma cells specifically resistant to Abeta25-35 cytotoxicity without affecting their vulnerability to serum deprivation. Together, nSMase activation with subsequent ceramide production may contribute, at least partially, to Abeta25-35 cytotoxicity in cell types with cerebral endothelial and glial lineage.
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------>authors2=Yeh CH
------>authors3=Chen S
------>authors4=Xu J
------>authors5=Hsu CY.
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------>authors=Yang DI
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------>updateTitle=Neutral sphingomyelinase activation in endothelial and glial cell death induced by amyloid beta-peptide.
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------>publish_year=2004
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A B C D E F G H I J K L M N O P Q R S T U V W X Y Z