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BioMed Research International
Volume 2013 (2013), Article ID 582526, 9 pages
http://dx.doi.org/10.1155/2013/582526
Research Article

Neurogenesis and Increase in Differentiated Neural Cell Survival via Phosphorylation of Akt1 after Fluoxetine Treatment of Stem Cells

1Stem Cell and Tissue Engineering Department, Research Center for Science and Technology in Medicine (RCSTiM), Tehran University of Medical Sciences, Tehran, Iran
2Faculty of Medicine, Islamic Azad University, Mashhad Branch, Mashhad 19988-96953, Iran
3Medical Nanotechnology Department, School of Advanced Technologies in Medicine, Tehran University of Medical Sciences, Tehran, Iran
4Rajaei Cardiovascular, Medical, and Research Centre, Iran University of Medical Sciences, P.O. Box 14185-615, Tehran, Iran

Received 10 April 2013; Revised 15 July 2013; Accepted 15 July 2013

Academic Editor: Paul Higgins

Copyright © 2013 Anahita Rahmani et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Fluoxetine (FLX) is a selective serotonin reuptake inhibitor (SSRI). Its action is possibly through an increase in neural cell survival. The mechanism of improved survival rate of neurons by FLX may relate to the overexpression of some kinases such as Akt protein. Akt1 (a serine/threonine kinase) plays a key role in the modulation of cell proliferation and survival. Our study evaluated the effects of FLX on mesenchymal stem cell (MSC) fate and Akt1 phosphorylation levels in MSCs. Evaluation tests included reverse transcriptase polymerase chain reaction, western blot, and immunocytochemistry assays. Nestin, MAP-2, and β-tubulin were detected after neurogenesis as neural markers. Ten μM of FLX upregulated phosphorylation of Akt1 protein in induced hEnSC significantly. Also FLX did increase viability of these MSCs. Continuous FLX treatment after neurogenesis elevated the survival rate of differentiated neural cells probably by enhanced induction of Akt1 phosphorylation. This study addresses a novel role of FLX in neurogenesis and differentiated neural cell survival that may contribute to explaining the therapeutic action of fluoxetine in regenerative pharmacology.