Stem Cell Research & Therapy (Sep 2018)

Human chorionic villous mesenchymal stem/stromal cells protect endothelial cells from injury induced by high level of glucose

  • Y. S. Basmaeil,
  • A. M. Al Subayyil,
  • T. Khatlani,
  • E. Bahattab,
  • M. Al-Alwan,
  • F. M. Abomaray,
  • B. Kalionis,
  • M. A. Alshabibi,
  • A. S. AlAskar,
  • M. H. Abumaree

DOI
https://doi.org/10.1186/s13287-018-0984-0
Journal volume & issue
Vol. 9, no. 1
pp. 1 – 19

Abstract

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Abstract Background Mesenchymal stem/stromal cells derived from chorionic villi of human term placentae (pMSCs) protect human endothelial cells from injury induced by hydrogen peroxide (H2O2). In diabetes, elevated levels of glucose (hyperglycaemia) induce H2O2 production, which causes the endothelial dysfunction that underlies the enhanced immune responses and adverse complications associated with diabetes, which leads to thrombosis and atherosclerosis. In this study, we examined the ability of pMSCs to protect endothelial cell functions from the negative impact of high level of glucose. Methods pMSCs isolated from the chorionic villi of human term placentae were cultured with endothelial cells isolated from human umbilical cord veins in the presence of glucose. Endothelial cell functions were then determined. The effect of pMSCs on gene expression in glucose-treated endothelial cells was also determined. Results pMSCs reversed the effect of glucose on key endothelial cell functions including proliferation, migration, angiogenesis, and permeability. In addition, pMSCs altered the expression of many genes that mediate important endothelial cell functions including survival, apoptosis, adhesion, permeability, and angiogenesis. Conclusions This is the first comprehensive study to provide evidence that pMSCs protect endothelial cells from glucose-induced damage. Therefore, pMSCs have potential therapeutic value as a stem cell-based therapy to repair glucose-induced vascular injury and prevent the adverse complications associated with diabetes and cardiovascular disease. However, further studies are necessary to reveal more detailed aspects of the mechanism of action of pMSCs on glucose-induced endothelial damage in vitro and in vivo.

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