A simple, sensitive and widely applicable ELISA for S100B: Methodological features of the measurement of this glial protein

Leite, Marina Concli; Galland, Fabiana; Brolese, Giovana; Guerra, Maria Cristina; Bortolotto, Josiane Woutheres; Freitas, Rodrigo Eduardo Orgo de; Almeida, Lúcia Maria Vieira de; Gottfried, Carmem; Gonçalves, Carlos Alberto

doi:10.1016/j.jneumeth.2007.11.021

Cited by 116 publications

(54 citation statements)

References 35 publications

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“…GS activity was expressed as µmol/h/mg protein and was expressed as a percentage of the control. S100B measurement S100B was measured by an enzyme-linked immunosorbent assay, as previously described (Leite et al 2008). Briefly, 50 μL of sample and 50 μL of Tris buffer were incubated for 2 h on a microtiter plate previously coated with monoclonal anti-S100B (SH-B1) antibody.…”

Section: Glutamine Synthetase (Gs) Activitymentioning

confidence: 99%

Methylglyoxal and carboxyethyllysine reduce glutamate uptake and S100B secretion in the hippocampus independently of RAGE activation

et al. 2015

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Diabetes is a metabolic disease characterized by high fasting-glucose levels. Diabetic complications have been associated with hyperglycemia and high levels of reactive compounds, such as methylglyoxal (MG) and advanced glycation endproducts (AGEs) formation derived from glucose. Diabetic patients have a higher risk of developing neurodegenerative diseases, such as Alzheimer's disease or Parkinson's disease. Herein, we examined the effect of high glucose, MG and carboxyethyllysine (CEL), a MG-derived AGE of lysine, on oxidative, metabolic and astrocyte-specific parameters in acute hippocampal slices, and investigated some of the mechanisms that could mediate these effects. Glucose, MG and CEL did not alter reactive oxygen species (ROS) formation, glucose uptake or glutamine synthetase activity. However, glutamate uptake and S100B secretion were decreased after MG and CEL exposure. RAGE activation and glycation reactions, examined by aminoguanidine and L-lysine co-incubation, did not mediate these changes. Acute MG and CEL exposure, but not glucose, were able to induce similar effects on hippocampal slices, suggesting that conditions of high glucose concentrations are primarily toxic by elevating the rates of these glycation compounds, such as MG, and by generation of protein cross-links. Alterations in the secretion of S100B and the glutamatergic activity mediated by MG and AGEs can contribute to the brain dysfunction observed in diabetic patients.

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Section: Glutamine Synthetase (Gs) Activitymentioning

confidence: 99%

Methylglyoxal and carboxyethyllysine reduce glutamate uptake and S100B secretion in the hippocampus independently of RAGE activation

et al. 2015

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“…ELISA for S100B ELISA for S100B was carried out, as described previously [22]. Briefly, 50 ll of sample plus 50 ll of Tris buffer were incubated for 2 h on a microtiter plate previously coated with monoclonal anti-S100B.…”

Section: Preparation and Incubation Of Hippocampal Slicesmentioning

confidence: 99%

S100B Secretion in Acute Brain Slices: Modulation by Extracellular Levels of Ca2+ and K+

et al. 2009

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Hippocampal slices have been widely used to investigate electrophysiological and metabolic neuronal parameters, as well as parameters of astroglial activity including protein phosphorylation and glutamate uptake. S100B is an astroglial-derived protein, which extracellularly plays a neurotrophic activity during development and excitotoxic insult. Herein, we characterized S100B secretion in acute hippocampal slices exposed to different concentrations of K(+) and Ca(2+) in the extracellular medium. Absence of Ca(2+) and/or low K(+) (0.2 mM KCl) caused an increase in S100B secretion, possibly by mobilization of internal stores of Ca(2+). In contrast, high K(+) (30 mM KCl) or calcium channel blockers caused a decrease in S100B secretion. This study suggests that exposure of acute hippocampal slices to low- and high-K(+) could be used as an assay to evaluate astrocyte activity by S100B secretion: positively regulated by low K(+) (possibly involving mobilization of internal stores of Ca(2+)) and negatively regulated by high-K(+) (likely secondary to influx of K(+)).

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“…Future studies in larger samples may focus on drug-naive schizophrenic subjects and the comparison of different standardized treatment regimens to further elucidate the suggested link between S100B and abnormal energy metabolism. The six genome-wide association studies (GWAS) completed in bipolar disorder (BD) [1][2][3][4][5][6] have revealed some promising association signals that have been replicated in independent study samples, 7 but the mechanism by which these genes increase disease susceptibility has remained unresolved. Here, our goal was (i) to replicate the best results from the study by Sklar et al, 2008 4 and also the highest ranking imputed SNPs from the WTCCC study 1 and (ii) to define the effect of the Figure 1 Elevated S100B serum concentrations (a) and an increased C-peptide/glucose ratio (b), indicating insulin resistance, were schizophrenia related.…”

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confidence: 99%

Elevated S100B levels in schizophrenia are associated with insulin resistance

et al. 2009

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A simple, sensitive and widely applicable ELISA for S100B: Methodological features of the measurement of this glial protein

Cited by 116 publications

References 35 publications

Methylglyoxal and carboxyethyllysine reduce glutamate uptake and S100B secretion in the hippocampus independently of RAGE activation

Methylglyoxal and carboxyethyllysine reduce glutamate uptake and S100B secretion in the hippocampus independently of RAGE activation

S100B Secretion in Acute Brain Slices: Modulation by Extracellular Levels of Ca2+ and K+

Elevated S100B levels in schizophrenia are associated with insulin resistance

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