Disease relevance of cerebroside

• These data implicate myelin basic protein as an encephalitogen in these autoimmune diseases of the human nervous system, but suggest that immune responses to cerebroside and certain gangliosides may have an augmentative role in severe disease [1].
• To perform large-scale multiplex analysis of antibody responses to lipids in multiple sclerosis, we developed microarrays composed of lipids present in the myelin sheath, including ganglioside, sulfatide, cerebroside, sphingomyelin and total brain lipid fractions [2].
• Antibody levels to the virus capsid antigen of the Epstein-Barr virus and to the brain cell antigens myelin and cerebroside were elevated during active CNS disease [3].
• Human saposin B deficiency, transmitted as an autosomal recessive trait, results in tissue accumulation of cerebroside sulfate and a clinical picture resembling metachromatic leukodystrophy (activator-deficient metachromatic leukodystrophy) [4].
• The follicle-associated epithelium covering human gut lymphoid follicles expresses CCR5, but not CXCR4, and lactosyl cerebroside, suggesting that HIV-1 infection may occur through M cells and enterocytes at these sites [5].

High impact information on cerebroside

• The level of antibody to cerebroside correlated best with the number of injections of vaccine, but like antibody to myelin basic protein, the antibody to cerebroside was present in the cerebrospinal fluid of patients with major complications [1].
• Stereotaxically guided administration of antibodies to cerebroside sulfate into the periaqueductal gray region, the most sensitive brain region in which to demonstrate inhibition of this response, antagonizes the effect of morphine and beta-endorphin [6].
• Autoradiographs showed a shift of radioactive grains from astroglia and arachnoidal cells to myelin, indicating that actively myelinating oligodendroglia incorporate [35S]sulfate into myelin sulfatide; there was a concomitant increase in the activity of cerebroside sulfotransferase [7].
• Saposin B is a small, nonenzymatic glycosphingolipid activator protein required for the breakdown of cerebroside sulfates (sulfatides) within the lysosome [8].
• Similarly, brain cerebroside levels remained low in HCT-treated twitcher mice [9].

Chemical compound and disease context of cerebroside

• The paradoxical findings of a severely reduced concentration of galactosylceramide and a primary deficiency of cerebroside-beta-galactosidase can be explained by the present finding of the accumulation of galactosylsphingosine in the brains from patients who had died from Krabbe disease [10].
• Type-I activation appears to involve bile salt interaction with substrate, while type-II activation appears to involve enzyme interaction with solid-phase cholic acid. the putative mutant arylsulphatase A in an unusual form of metachromatic leukodystrophy hydolysed cerebroside sulphate only in the presence of high levels of cholate [11].
• A case of globoid cell leukodystrophy (Krabbe's disease) was diagnosed prenatally by demonstrating a profound deficiency of cerebroside beta-galactosidase in cultured amniotic cells [12].
• To better define the sphingolipid metabolism during focal brain ischemia, levels of ceramide, sphingomyelin, cerebroside and gangliosides were determined in rat cerebral cortex during focal ischemia produced by occlusion of the middle cerebral artery [13].
• Influence of reduced cholesterol synthesis on the activity of cerebroside sulfotransferase in cultured glioblastoma cells treated with estradiol [14].

Biological context of cerebroside

• Nevertheless, the hydrolysis of cerebroside sulfate by growing fibroblasts was markedly attenuated [15].
• Competitive binding of dynorphin-(1-13) and beta-endorphin to cerebroside sulfate in solution [16].
• Treatment of rice leaves with cerebroside A induced the accumulation of antimicrobial compounds (phytoalexins), cell death, and increased resistance to subsequent infection by compatible pathogens [17].
• We have identified a novel galactose 3-O-sulfotransferase, termed Gal3ST-4, by analysis of an expression sequence tag using the amino acid sequence of human cerebroside 3'-sulfotransferase (Gal3ST-1) [18].
• A novel sulfotransferase gene (designated GP3ST) was identified on human chromosome 2q37.3 based on its similarity to the cerebroside 3'-sulfotransferase (CST) cDNA (Honke, K., Tsuda, M., Hirahara, Y., Ishii, A., Makita, A., and Wada, Y. (1997) J. Biol. Chem. 272, 4864-4868) [19].

Anatomical context of cerebroside

• At later times the plasma membrane became visibly labeled as well, at which point 90% of the cell-associated fluorescence was recovered as NBD-labeled sphingomyelin and NBD-labeled cerebroside [20].
• On the other hand, levels of cerebroside were approximately 35% of control values in sciatic nerve, remained about the same in the brain, and were elevated 10-fold in the kidney of twitcher mice [9].
• The cerebellar cortex, corpus striatum, and thalamus in Gaucher brains had mildly increased levels of glucocerebroside, especially when the values were expressed as a percentage of total non-hydroxy fatty-acid cerebroside [21].
• They were neither induced by nor cross-reacting with cerebroside and peripheral nervous system (PNS) tissue [22].
• The incorporation of cerebroside sulfate or phosphatidylserine by N18TG2 cells did not increase the number of opiate binding sites in this cell line as determined by [3H]naloxone, [3H]etorphine, or 3H-labeled D-Ala2-Met5-enkephalinamide binding [23].

Associations of cerebroside with other chemical compounds

• Large spherical liposomes, small spherical liposomes, and long tubular liposomes are formed, depending on the relative acyl chain lengths of the phosphatidylcholine and cerebroside [24].
• Carbon 13 NMR spectroscopy of a cerebroside. Proof of the beta-pyranosyl structure of D-glucosylceramide [25].
• Identical treatment of N18TG2 cells with cerebroside or psychosine sulfate did not produce any potentiation of the opiate inhibition of adenylate cyclase [23].
• During remyelination, expression of myelin-related mRNA species, as well as cerebroside and cholesterol synthesis were restored to normal [26].
• These results, along with the invariance of GalCer structure obtained by a Fourier analysis of the X-ray data, indicated that there was an extremely narrow fluid space (less than the diameter of a single water molecule) between fully hydrated cerebroside bilayers [27].

Gene context of cerebroside

• Cb supported CG8 neurons at about 55% of the plateau value achieved with CNTF, but had hardly any effect on the other neuron populations tested [28].
• No patient had antibody to proteolipid protein, myelin-associated glycoprotein, or cerebroside [29].
• Molecular cloning and characterization of the mouse CGT gene encoding UDP-galactose ceramide-galactosyltransferase (cerebroside synthetase) [30].
• Inhibition of PKC with calphostin C and cerebroside completely blocked growth cone formation, whereas the inhibition of PTK with erbstatin analog significantly reduced growth cone formation [31].
• Cerebroside formation in the peripheral nervous system of normal and Trembler mice [32].

Analytical, diagnostic and therapeutic context of cerebroside

• Circular dichroism was used as a probe for competitive binding of two opioid peptides, dynorphin-(1-13) and beta-endorphin, with cerebroside sulfate, a membrane lipid thought to be part of the morphine receptor complex [16].
• Special attention was paid to contamination with brain tissue, which was assessed by luxol staining and cerebroside assays for myelin and by scanning electron microscopy [33].
• Bovine brain cerebrosides (BOV-CER) were separated by high-performance liquid chromatography into cerebroside fractions with a single acyl chain type or with a relatively homogeneous acyl chain distribution [34].
• The thermal behavior of these isolated cerebroside fractions was studied by differential scanning calorimetry [34].
• Nutritional rehabilitation up to 60 days of age subsequent to malnutrition for the first 30 days fully corrected the ganglioside pattern, but not the molar ratio, of the major lipids (because of persistent deficit in cerebroside + sulphatide) and the composition of the phospholipids (because of small but significant deficit of SPh) [35].

References