Ganglioside GM1 Protection from Apoptosis of Rat Heart Fibroblasts

Ceramide is involved as a mediator of apoptosis induced by a variety of signaling molecules or stressful events. Ceramide-derived sphingosine 1-phosphate behaves as an antiapoptotic agent. The ganglioside GM1 is known to protect neuronal cell lines from apoptosis induced by serum/growth factor withd...

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Bibliographic Details
Published in:Archives of biochemistry and biophysics 1999-10, Vol.370 (2), p.156-162
Main Authors: Cavallini, Lucia, Venerando, Rina, Miotto, Giovanni, Alexandre, Adolfo
Format: Article
Language:English
Subjects:
Animals
apoptosis
Apoptosis - drug effects
Apoptosis - physiology
Cells, Cultured
ceramide
Enzyme Activation - drug effects
Enzyme Inhibitors - pharmacology
Fibroblasts - cytology
Fibroblasts - drug effects
Fibroblasts - metabolism
G(M1) Ganglioside - metabolism
G(M1) Ganglioside - pharmacology
ganglioside
Heart - drug effects
heart fibroblasts
Lysophospholipids
Myocardium - cytology
Myocardium - metabolism
Phosphotransferases (Alcohol Group Acceptor) - antagonists & inhibitors
Phosphotransferases (Alcohol Group Acceptor) - metabolism
Rats
Second Messenger Systems
Sphingosine - analogs & derivatives
Sphingosine - biosynthesis
Sphingosine - pharmacology
sphingosine 1P
staurosporine
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Summary:Ceramide is involved as a mediator of apoptosis induced by a variety of signaling molecules or stressful events. Ceramide-derived sphingosine 1-phosphate behaves as an antiapoptotic agent. The ganglioside GM1 is known to protect neuronal cell lines from apoptosis induced by serum/growth factor withdrawal and its effect is mediated in part by the direct activation of the trkA NGF receptor [G. Ferrari et al. (1995) J. Biol. Chem. 270, 3074–3080]. We show that GM1, similarly to sphingosine 1-phosphate, protects rat heart fibroblasts from apoptosis induced by the protein kinase C inhibitor staurosporine and by C2-ceramide. Furthermore, we show that GM1 induces the synthesis of sphingosine 1-phosphate and that this effect is partially prevented by the sphingosine kinase inhibitor N,N-dimethylsphingosine. We conclude that the antiapoptotic action of GM1 is largely to be ascribed to an increased sphingosine kinase activity.
ISSN:0003-9861
1096-0384
DOI:10.1006/abbi.1999.1378