1. The protective effects of umbilical cord-derived endothelial colony forming cells on hepatic veno-occlusive disease.
- Author
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Chen L, Zhang J, Liu X, Yao M, and Zhang H
- Subjects
- Animals, Cell Movement drug effects, Cells, Cultured, Chemical and Drug Induced Liver Injury prevention & control, Chemokine CXCL12 metabolism, China, Endothelial Cells metabolism, Hepatic Veno-Occlusive Disease metabolism, Hepatic Veno-Occlusive Disease pathology, Human Umbilical Vein Endothelial Cells physiology, Humans, Liver pathology, Male, Mice, Mice, Inbred NOD, Receptors, CXCR metabolism, Receptors, CXCR4 metabolism, Umbilical Cord cytology, Hepatic Veno-Occlusive Disease therapy, Human Umbilical Vein Endothelial Cells metabolism
- Abstract
Hepatic veno-occlusive disease (HVOD) characterized by endothelial cell dysfunction is one of the serious complications after hematopoietic stem-cell transplantation or chemotherapeutic drug application. The mortality of HVOD patients with multiorgan dysfunction is as high as 80%. The primary aim of this study was to evaluate whether the infusion of human umbilical cord-derived endothelial colony forming cells (hUC-ECFCs) could mitigate HVOD injury and investigate the underlying mechanism. We found that the expression of chemokine C-X-C chemokine ligand 12 (CXCL12) was markedly increased in the livers of HVOD mice. Meanwhile, hUC-ECFCs infusion could significantly ameliorate liver injury in HVOD mice, which was accompanied by hUC-ECFCs recruitment in the liver, reduced liver pathological alterations, and decreased serum alanine aminotransferase and aspartate aminotransferase activity. Besides, CXCL12-induced migration in hUC-ECFCs was partly impeded by chemokine receptor type 7 (CXCR7) silence or CXCR4 blockage. In conclusion, our results demonstrated that hUC-ECFCs could mitigate HVOD through homing to the injured liver via the CXCL12-CXCR4/CXCR7 signaling pathway., (© 2020 International Federation for Cell Biology.)
- Published
- 2020
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