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Astroglial S100B Secretion Is Mediated by Ca2+ Mobilization from Endoplasmic Reticulum: A Study Using Forskolin and
Marina C Leite1, Fabiana Galland2, Maria Cristina Guerra1
1Departamento de Bioquímica, Universidade Federal do Rio Grande do Sul, Ramiro Barcelos, 2600-Anexo, Porto Alegre 90035-003, RS, Brazil.
International Journal of Molecular Sciences
|December 9, 2023
Summary
Dimethyl sulfoxide (DMSO) triggers the release of S100B protein from astrocytes by increasing intracellular calcium. This calcium mobilization, originating from the endoplasmic reticulum, is key to S100B secretion.
Area of Science:
- Neuroscience
- Cell Biology
- Biochemistry
Background:
- S100B protein is secreted by astrocytes and serves as a glial marker for neurological conditions.
- The precise mechanism of S100B secretion remains largely unknown.
- Dimethyl sulfoxide (DMSO) is a common solvent in biological research.
Purpose of the Study:
- To investigate the role of intracellular calcium in S100B secretion from astrocytes.
- To determine the effect of DMSO on S100B secretion.
- To elucidate the mechanism of astroglial S100B release.
Main Methods:
- Primary astrocyte cultures were utilized for in vitro experiments.
- Real-time fluorescence microscopy was employed to measure intracellular calcium dynamics.
- In vivo studies involved Wistar rats and ex vivo hippocampal slices to assess DMSO's effect.
Main Results:
- DMSO was identified as a potent S100B secretagogue, inducing a biphasic intracellular calcium response.
- Astroglial S100B secretion is stimulated by elevated intracellular calcium, primarily mobilized from the endoplasmic reticulum.
- Inhibition of plasma membrane calcium channels reduced S100B secretion, indicating the importance of calcium replenishment.
- DMSO-induced S100B secretion was validated in vivo and in ex vivo brain slices.
Conclusions:
- Astroglial S100B secretion is regulated by intracellular calcium levels.
- The findings suggest a non-vesicular, calcium-modulated export mechanism for S100B.
- This study provides insights into the molecular mechanisms governing S100B release from astrocytes.
