Title:S100b Induces Expression of Myoglobin in APβ Treated Neuronal Cells In Vitro: A Possible Neuroprotective Mechanism
VOLUME: 9 ISSUE: 4
Author(s):Maria E. Clementi, Beatrice Sampaolese and Bruno Giardina
Affiliation:CNR-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.
Keywords:S100b, oxidative stress, myoglobin.
Abstract:Background: In this study, human neuroblastoma cells (IMR32)
treated with Amyloid Beta Peptide (APβ), were used as model to evaluate the
molecular basis of protective role of S100b, a neurotrophic factor and neuronal
survival protein, highly expressed by reactive astrocytes close to amyloid deposition
in the cortex of Alzheimer's patients. The aim of this work is to value the
effect of S100b on ROS production in cells treated with Amyloid Beta Peptide
and the subsequent influence on globin gene expression.
Method: In this study we investigated the effect of S100b on ROS production and
on globin gene expression in human neuroblastoma cells (IMR32) treated with
Amyloid Beta Peptide (APβ).
Results: Our results have shown that at nanomolar concentrations, S100b protects cells against AP
mediated cytotoxicity and the protective mechanism could be related, almost in part, to the control
of ROS production through an over expression of Myoglobin gene.
Conclusion: In light of our results, we speculate that over-expression of the Myoglobin gene could
be read as a possible attempt of the cell to increase the scavengers of reactive oxygen species (ROS).
