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Effect of Leukemia Inhibitory Factor on the Myelinogenic Ability of Schwann-Like Cells Induced From Human Adipose-Derived Stem Cells Publisher Pubmed



Razavi S1 ; Mardani M1 ; Kazemi M1 ; Esfandiari E1 ; Narimani M1 ; Esmaeili A2 ; Ahmadi N3
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Authors Affiliations
  1. 1. Department of Anatomical Sciences and Molecular Biology, School of Medicine, Isfahan University of Medical Sciences, 81744-176 Isfahan, Iran
  2. 2. Department of Biology, Faculty of Sciences, University of Isfahan, Isfahan, Iran
  3. 3. Department of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran

Source: Cellular and Molecular Neurobiology Published:2013


Abstract

The Schwann cells (SCs) may be obtain from nerve biopsies for autologous transplantation. However, it is difficult to obtain sufficient amount of SCs for clinical applications. Human adipose-derived stem cells (ADSCs) can be induced to differentiate into Schwann-like cells (S-like cells) and used for autologous transplantation. However, effect of leukemia inhibitory factor (LIF) on the myelinogenic ability of SC-like cells induced from human ADSC is not investigated yet. The aim of this study was to evaluate of the effect of exogenous LIF on myelinogenic potential of differentiated cells in vitro. ADSCs were harvested from human fat tissue and characterized using flow cytometry. Human ADSCs were treated for sphere formation and LIF was added to terminal differentiation medium. GFAP/S100β and MBP markers were used to confirm differentiation of human ADSCs, and myelinogenic ability of SC-like cells, respectively, using both immunostaining and real-time RT-PCR analysis. The analysis for GFAP+/S100β+ revealed that LIF can increase both differentiated cells rates and the percentage of myelinating SC-like cells (p < 0.05). Our data showed that SC-like cells induced from human ADSCs were able to generate myelin when exposed to LIF and these cells could be a potential source for the treatment of peripheral and central axonal injuries. © 2012 Springer Science+Business Media New York.
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