Human decidua basalis mesenchymal stem/stromal cells protect endothelial cell functions from oxidative stress induced by hydrogen peroxide and monocytes

M. A. Alshabibi, T. Khatlani, F. M. Abomaray, A. S. AlAskar, B. Kalionis, S. A. Messaoudi, R. Khanabdali, A. O. Alawad, M. H. Abumaree
2018 Stem Cell Research & Therapy  
Human decidua basalis mesenchymal stem/multipotent stromal cells (DBMSCs) inhibit endothelial cell activation by inflammation induced by monocytes. This property makes them a promising candidate for cell-based therapy to treat inflammatory diseases, such as atherosclerosis. This study was performed to examine the ability of DBMSCs to protect endothelial cell functions from the damaging effects resulting from exposure to oxidatively stress environment induced by H 2 O 2 and monocytes. Methods:
more » ... nocytes. Methods: DBMSCs were co-cultured with endothelial cells isolated from human umbilical cord veins in the presence of H 2 O 2 and monocytes, and various functions of endothelial cell were then determined. The effect of DBMSCs on monocyte adhesion to endothelial cells in the presence of H 2 O 2 was also examined. In addition, the effect of DBMSCs on HUVEC gene expression under the influence of H 2 O 2 was also determined. Results: DBMSCs reversed the effect of H 2 O 2 on endothelial cell functions. In addition, DBMSCs reduced monocyte adhesion to endothelial cells and also reduced the stimulatory effect of monocytes on endothelial cell proliferation in the presence of H 2 O 2 . Moreover, DBMSCs modified the expression of many genes mediating important endothelial cell functions. Finally, DBMSCs increased the activities of glutathione and thioredoxin reductases in H 2 O 2 -treated endothelial cells. Conclusions: We conclude that DBMSCs have potential for therapeutic application in inflammatory diseases, such as atherosclerosis by protecting endothelial cells from oxidative stress damage. However, more studies are needed to elucidate this further.
doi:10.1186/s13287-018-1021-z fatcat:ld7ig6eoz5fhjhxk7gezs2wlpe