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S100b Induces Expression of Myoglobin in APβ Treated Neuronal Cells In Vitro: A Possible Neuroprotective Mechanism
Maria E Clementi1, Beatrice Sampaolese, Bruno Giardina
1CNR-ICRM Institute of "Chimica del Riconoscimento Molecolare", c/o Institute of Biochemistry and Clinical Biochemistry, Catholic University Medical School, Largo F. Vito 1, 00168 Rome, Italy.
Current Aging Science
|February 23, 2016
Summary
The neurotrophic factor S100b protects against Amyloid Beta Peptide (APβ) toxicity by reducing reactive oxygen species (ROS) production, partly through Myoglobin gene overexpression.
Area of Science:
- Neuroscience
- Molecular Biology
- Cell Biology
Background:
- Alzheimer's disease pathology involves amyloid plaques and reactive astrocytes.
- S100b is a neurotrophic factor and neuronal survival protein upregulated by astrocytes near amyloid deposits.
- Amyloid Beta Peptide (APβ) induces cellular stress, including reactive oxygen species (ROS) production.
Purpose of the Study:
- To investigate the protective role of S100b in APβ-treated neuroblastoma cells.
- To determine the effect of S100b on ROS production and globin gene expression.
- To elucidate the molecular mechanisms underlying S100b's neuroprotective effects.
Main Methods:
- Utilized human neuroblastoma IMR32 cells as a model system.
- Treated cells with Amyloid Beta Peptide (APβ) and varying concentrations of S100b.
- Assessed ROS production and globin gene expression levels.
Main Results:
- Nanomolar concentrations of S100b demonstrated a protective effect against APβ-mediated cytotoxicity.
- S100b's protective mechanism is partly attributed to the control of ROS production.
- Observed an overexpression of the Myoglobin gene in response to S100b treatment.
Conclusions:
- S100b exhibits neuroprotective properties against APβ-induced cellular damage.
- Myoglobin gene overexpression may serve as a cellular defense mechanism against ROS.
- S100b's modulation of ROS and gene expression offers insights into Alzheimer's disease pathogenesis.
