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Publication Details

Title :

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

Journal:

Stem Cell Res Ther.

Impact Factor:

4.963

Authors:

Basmaeil YS1, Al Subayyil AM1, Khatlani T1, Bahattab E2, Al-Alwan M3, Abomaray FM4,5, Kalionis B6, Alshabibi MA1, AlAskar AS1,7,8, Abumaree MH9,10.

Affiliations:

1 Stem Cells and Regenerative Medicine Department, King Abdullah International Medical Research Centre, King Abdulaziz Medical City, Ministry of National Guard Health Affairs, P.O. Box 22490, Mail Code 1515, Riyadh, 11426, Saudi Arabia.

2 National Center for Stem Cell Technology, Life Sciences and Environment Research Institute, King Abdulaziz City for Science and Technology, P.O. Box 6086, Riyadh, 11442, Saudi Arabia.

3 Stem Cell and Tissue Re-Engineering Program, King Faisal Specialist Hospital and Research Centre, Collage of Medicine, Al-Faisal University, MBC-03, P.O. Box 3354, Riyadh, 11211, Saudi Arabia.

4 Division of Obstetrics and Gynecology, Department of Clinical Science, Intervention and Technology, Karolinska Institutet, 14186, Stockholm, Sweden.

5 Center for Hematology and Regenerative Medicine, Karolinska Institutet, 14186, Stockholm, Sweden.

6 Department of Maternal-Fetal Medicine Pregnancy Research Centre and University of Melbourne Department of Obstetrics and Gynaecology, Royal Women’s Hospital, Parkville, VIC, 3052, Australia.

7 College of Medicine, King Saud Bin Abdulaziz University for Health Sciences, King Abdulaziz Medical City, Ministry of National Guard Health Affairs, P.O. Box 3660, Mail Code 3124, Riyadh, 11481, Saudi Arabia.

8 Adult Hematology and Stem Cell Transplantation, King Abdulaziz Medical City, Ministry of National Guard Health Affairs, P.O. Box 22490, Mail Code 1515, Riyadh, 11426, Saudi Arabia.

9 Stem Cells and Regenerative Medicine Department, King Abdullah International Medical Research Centre, King Abdulaziz Medical City, Ministry of National Guard Health Affairs, P.O. Box 22490, Mail Code 1515, Riyadh, 11426, Saudi Arabia. mohamedabumaree@hotmail.com.

10 College of Science and Health Professions, King Saud Bin Abdulaziz University for Health Sciences, King Abdulaziz Medical City, Ministry of National Guard Health Affairs, P.O. Box 3660, Mail Code 3124, Riyadh, 11481, Saudi Arabia. mohamedabumaree@hotmail.com.

Year of Publication:

2018

DOI:

10.1186/s13287-018-0984-0

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.