Current Issue

Volume 20, Number 2, Summer 2018, Serial Number: 78 Pages: 259-266

Prostaglandin F-2α Stimulates The Secretion of Vascular Endothelial Growth Factor and Induces Cell Proliferation and Migration of Adipose Tissue Derived Mesenchymal Stem Cells


Abdolkhaleg Deezagi, Ph.D., , *, Samira Shomali, M.Sc., ,
Department of Molecular Medicine and Biochemistry, National Institute of Genetic Engineering and Biotechnology, Tehran, Iran
*Corresponding Address: P.O.Box: 14155-6343 Department of Molecular Medicine and Biochemistry National Institute of Genetic Engineering and Biotechnology Km. 17 Karaj Tehran Email:deezagi@nigeb.ac.ir

Abstract

Objective

Tissue engineering today uses factors that can induce differentiation of mesenchymal stem cells (MSCs) into other cell types. However, the problem of angiogenesis in this differentiated tissue remains an unresolved area of research interest. The aim of this study was to investigate the effects of prostaglandin F-2α (PGF-2α) on the expression of vascular endothelial growth factor (VEGF) in human adipose tissue derived MSCs.

Materials and Methods

In this experimental research, human adipose tissue was digested using collagenase. The isolated MSCs cells were treated with PGF-2α (up to 5 μg/ml) and incubated for 96 hours. Cell proliferation, secretion of VEGF and cell migration were spontaneously assayed by MTT, BrdU, ELISA, RT-PCR and scratching methods.

Results

Cell growth at 1.0, 2.5, 5 µg/ml of PGF-2α was not significantly reduced compared to control cells, suggesting that these concentrations of PGF-2α are not toxic to cell growth. The results of the BrdU incorporation assay indicated that, in comparison to untreated cells, BrdU incorporation was respectively 1.08, 1.96, 2.0 and 1.8 fold among cells treated with 0.1, 1.0, 2.5 and 5.0 µg/ml of PGF-2α. The scratching test also demonstrated a positive influence on cell proliferation and migration. Cells treated with 1.0 µg/ml of PGF-2α for 12 hours showed the highest relative migration and coverage in comparison to untreated cells. Quantitative VEGF ELISA and RT- PCR results indicated an increase in VEGF expression and secretion in the presence of PGF-2α. The amount of VEGF produced in response to 0.1, 1.0, 2.5 and 5.0 µg/ml of PGF-2α was 62.4 ± 3.2 , 66.3 ± 3.7, 53.1 ± 2.6 and 49.0 ± 2.3 pg/ml, respectively, compared to the 35.2 ± 2.1 pg/ml produced by untreated cells.

Conclusion

Stimulation of VEGF secretion by PGF-2α treated MSCs could be useful for the induction of angiogenesis in tissue engineering in vitro.