S100b Induces Expression of Myoglobin in APB Treated Neuronal Cells In Vitro: A Possible Neuroprotective Mechanism

In this study, human neuroblastoma cells (IMR32) treated with Amyloid Beta Peptide (AP?, 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 nearby of 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. Our results 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. In conclusions, in light of these 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).