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

[ Vol. 9 , Issue. 4 ]

Author(s):

Maria E. Clementi, Beatrice Sampaolese and Bruno Giardina   Pages 279 - 283 ( 5 )

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).

Keywords:

S100b, oxidative stress, myoglobin.

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.

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