Transduction of Mesenchymal Stem Cells that Express VEGF-A and Pre-conditioning with SDF1α In order to Increase Survival for use in Myocardial Infarction Treatment in a Rat Model

Authors
R. Esmaeili 1
K. Majidzadeh-A 2, 3
L. Eini 2
P. Hoseinpour 4
A. Teymourzadeh 2
M. Sadeghizadeh 5
M. Sadeghizadeh 5
1 Department of Genetics, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran
2 Department of Cancer Genetics, Breast Cancer Research Center, ACECR, Tehran, Iran
3 Tasnim Biotechnology Research Center (TBRC), Faculty of Medicine, AJA University of Medical Sciences, Tehran, Iran
4 Breast Cancer Research Center, ACECR, Tehran, Iran
5 Department of Molecular Genetics, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran
Abstract
Objective: The use of stem cells, particularly mesenchymal stem cells (MSCs), with genes and various growth factors as treatments for myocardial infarction and various other diseases is highly regarded. However these cells meet with inflammation and a hypoxic environment in the target tissue. Hence, treatment with factors that increase the resistance of these stem cells is of importance. Stem cells also can be used as carriers for gene therapy. The aim of the present research is to produce VEGF expressing MSCs. We investigate the effect of stromal derived factor 1 on MSC survival in order to use these cells in a future rat myocardial infarction model.
Methods: MSCs were purified from young male rats by aspirating the cavity of femurs and tibias. After characterization, MSCs were transduced with VEGF using lipofectamine. Expression and function of VEGF was confirmed. Next, we treated MSCs with SDF1α at various time points. The effect of this chemokine was investigated using the LDH assay and by viable cell counts.
Results: The experiments confirmed the production and function of VEGF by MSCs. The LDH levels decreased significantly in SDF1α treated MSCs. Cell viability increased significantly in the presence of this chemokine.
Conclusion: Treatment of MSCs with the SDF1α chemokine has increased the survival of these cells. These MSCs are proper candidates for increasing angiogenesis and for further analysis in a rat model of myocardial infarction.

Keywords

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Pathobiology Reserach
Volume 18, Issue 3
October 2015
Pages 45-58