ArticleThe Biochemical journal2003
Lyso-glycosphingolipids mobilize calcium from brain microsomes via multiple mechanisms.
Article in The Biochemical journal, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 42 citations in OpenAlex.
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- Glucosylceramide and galactosylceramide, small glycosphingolipids with significant impact on health and disease.Glycobiology · 2021Review
- Substrate Reduction Therapy for Sandhoff Disease through Inhibition of Glucosylceramide Synthase Activity.Molecular therapy : the journal of the American Society of Gene Therapy · 2019Article
- A saposin deficiency model in Drosophila: Lysosomal storage, progressive neurodegeneration and sensory physiological decline.Neurobiology of disease · 2017Article
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- Lysosomal Re-acidification Prevents Lysosphingolipid-Induced Lysosomal Impairment and Cellular Toxicity.PLoS biology · 2016Article
- Psychosine-triggered endomitosis is modulated by membrane sphingolipids through regulation of phosphoinositide 4,5-bisphosphate production at the cleavage furrow.Molecular biology of the cell · 2016Article
- A new glucocerebrosidase-deficient neuronal cell model provides a tool to probe pathophysiology and therapeutics for Gaucher disease.Disease models & mechanisms · 2016Article
- Acidic CaMessenger (Los Angeles, Calif. : Print) · 2016Article
- Unbiased Cell-based Screening in a Neuronal Cell Model of Batten Disease Highlights an Interaction between Ca2+ Homeostasis, Autophagy, and CLN3 Protein Function.The Journal of biological chemistry · 2015Article
- Role of extracellular calcium and mitochondrial oxygen species in psychosine-induced oligodendrocyte cell death.Cell death & disease · 2014Article
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- Multi-system disorders of glycosphingolipid and ganglioside metabolism.Journal of lipid research · 2010Review
- Specific saposin C deficiency: CNS impairment and acid beta-glucosidase effects in the mouse.Human molecular genetics · 2010Article
- Glucosylceramide transfer from lysosomes--the missing link in molecular pathology of glucosylceramidase deficiency: a hypothesis based on existing data.Journal of inherited metabolic disease · 2006Article
- Upregulation of proinflammatory cytokines in the fetal brain of the Gaucher mouse.Journal of Korean medical science · 2006Article
- Down-regulation of Bcl-2 in the fetal brain of the Gaucher disease mouse model: a possible role in the neuronal loss.Journal of human genetics · 2004Article
- Glycosphingolipidoses: beyond the enzymatic defect.Glycoconjugate journal · 2004Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recently, we demonstrated that the GSL (glycosphingolipid), GlcCer (glucosylceramide), modulates Ca2+ release from intracellular stores and from microsomes by sensitizing the RyaR (ryanodine receptor), a major Ca2+-release channel of the endoplasmic reticulum, whereas the lyso derivative of GlcCer, namely GlcSph (glucosylsphingosine), induced Ca2+ release via a mechanism independent of the RyaR [Lloyd-Evans, Pelled, Riebeling, Bodennec, de-Morgan, Waller, Schiffmann and Futerman (2003) J. Biol. Chem. 278, 23594-23599]. We now systematically examine the mechanism by which GlcSph and other lyso-GSLs modulate Ca2+ mobilization from rat brain cortical and cerebellar microsomes. GlcSph, lactosylsphingosine and galactosylsphingosine all mobilized Ca2+, but at significantly higher concentrations than those required for GlcCer-mediated sensitization of the RyaR. GlcSph-induced Ca2+ mobilization was partially blocked by heparin, an inhibitor of the Ins(1,4,5) P3 receptor, and also partially blocked by thapsigargin or ADP, inhibitors of SERCA (sarcoplasmic/endoplasmic reticulum Ca2+-ATPase), but completely blocked when both acted together. In contrast, neither lactosylsphingosine nor galactosylsphingosine had any effect on Ca2+ release via either the Ins(1,4,5) P3 receptor or SERCA, but acted as agonists of the RyaR. Finally, and surprisingly, all three lyso-GSLs reversed inhibition of SERCA by thapsigargin. We conclude that different lyso-GSLs modulate Ca2+ mobilization via different mechanisms, and discuss the relevance of these findings to the GSL storage diseases in which lyso-GSLs accumulate.
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