Human Decidua Basalis mesenchymal stem/stromal cells reverse the damaging effects of high level of glucose on endothelial cells in vitro. Issue 4 (5th June 2020)

• Record Type: Journal Article
• Authors: Basmaeil, Yasser S.; Bahattab, Eman.; Alshabibi, Manal A.; Abomaray, Fawaz M.; Abumaree, Mohamed; Khatlani, Tanvir
• Is Part Of: Journal of cellular and molecular medicine. Volume 25:Issue 4(2021)
• Page Start: 1838
• Page End: 1850
• Publication Date: 2020-06-05
• Subjects: Decidua Basalis MSCs -- endothelial cell function -- gene expression -- glucose; Cytology; Medicine; Molecular Biology; Cytologie -- Périodiques; Médecine -- Périodiques; Biologie moléculaire -- Périodiques; Cytology -- Periodicals; Medicine -- Periodicals; Molecular biology -- Periodicals; 611.01805
• DOI: 10.1111/jcmm.15248
• Languages: English
• ISSNs: 1582-1838

Abstract

Abstract: Recently, we reported the therapeutic potential of mesenchymal stem/stromal cells (MSCs) from the maternal decidua basalis tissue of human term placenta (DBMSCs) to treat inflammatory diseases, such as atherosclerosis and cancer. DMSCs protect endothelial cell functions from the negative effects of oxidative stress mediators including hydrogen peroxide (H2 O2 ) and monocytes. In addition, DBMSCs induce the generation of anti‐cancer immune cells known as M1 macrophages. Diabetes is another inflammatory disease where endothelial cells are injured by H2 O2 produced by high level of glucose (hyperglycaemia), which is associated with development of thrombosis. Here, we investigated the ability of DBMSCs to reverse the damaging effects of high levels of glucose on endothelial cells. DBMSCs and endothelial cells were isolated from human placental and umbilical cord tissues, respectively. Endothelial cells were incubated with glucose in presence of DBMSCs, and their functions were evaluated. The effect of DBMSCs on glucose‐ treated endothelial cell expression of genes was also determined. DBMSCs reversed the effects of glucose on endothelial cell functions including proliferation, migration, angiogenesis and permeability. In addition, DBMSCs modified the expression of several genes mediating essential endothelial cell functions including survival, apoptosis, permeability and angiogenesis. We report the first evidence that DBMSCs protect the functions of endothelial cells from the damaging effects of glucose. Based on these results, we establish that DBMSCs are promising therapeutic agents to repair glucose‐induced endothelial cell injury in diabetes. However, these finding must be investigated further to determine the pathways underlying the protective role of DBMSCs on glucose‐stimulated endothelial cell Injury.