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S100B content and secretion decrease in astrocytes cultured in high-glucose medium.

Patrícia Nardin¹, Francine Tramontina, Marina C Leite

¹Departamento de Bioquímica, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Ramiro Barcelos, 2600-Anexo, 90035-003 Porto Alegre, RS, Brazil.

Neurochemistry International

|March 14, 2007

Summary

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High glucose levels impair astrocyte function, reducing S100B secretion, which may impact neuronal survival and contribute to cognitive deficits in diabetes.

Area of Science:

Neuroscience
Cell Biology
Biochemistry

Background:

S100B is an astrocyte calcium-binding protein regulating cytoskeleton and cell cycle.
Extracellular S100B influences neuronal survival (trophic or apoptotic effects) based on concentration.
Hyperglycemia in rats alters glial parameters, including S100B expression.

Purpose of the Study:

Investigate effects of high-glucose medium on primary cortical astrocytes and C6 glioma cells.
Analyze changes in cell density, morphology, and biochemical markers.
Compare S100B secretion profiles between primary astrocytes and glioma cells under hyperglycemic conditions.

Main Methods:

Culturing primary cortical astrocytes and C6 glioma cells in high-glucose medium.
Assessing cell density, morphology, and S100B and glial fibrillary acidic protein (GFAP) content.

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Measuring glutathione content and cell proliferation rates.

Analyzing S100B secretion patterns.

Main Results:

High-glucose environment reduced S100B, GFAP, glutathione content, and proliferation in both cell types.
Primary astrocytes showed decreased S100B secretion, while C6 glioma cells exhibited increased secretion.
Observed contrasting S100B secretion profiles in high-glucose conditions.

Conclusions:

Chronic hyperglycemia negatively impacts astrocyte function, decreasing extracellular S100B secretion.
Reduced S100B secretion by astrocytes may affect neuronal activity and survival.
Astrocyte alterations in diabetes could contribute to cognitive deficits and other impairments.