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Human Cord Blood-Endothelial Progenitor Cells Alleviate Intimal Hyperplasia of Arterial Damage in a Rat Stroke Model. | LitMetric

AI Article Synopsis

  • * The research evaluated the effects of hCB-EPCs on endothelial health after stent-induced arterial damage, observing different repair outcomes based on the presence or absence of these cells and varying recovery times (3 and 28 days).
  • * Results indicated that while stroke volume didn't differ significantly, hCB-EPC treatment reduced intimal hyperplasia and improved beneficial factors like VEGF and eNOS, ultimately promoting better healing and less inflammation in artery walls.

Article Abstract

Human cord blood-endothelial progenitor cells (hCB-EPCs) isolated from the human umbilical cord can be used to repair damaged arteries. In this study, we used an animal model with pathological changes that mimics artery wall damage caused by stent retrievers in humans. We injected hCB-EPCs to investigate their effect on endothelial hyperplasia and dysfunction during intimal repair. Four groups were established based on the length of reperfusion (3 and 28 days), as well as the presence or absence of hCB-EPC therapy. Damage to the internal carotid artery was evaluated by hematoxylin-eosin and immunohistochemical staining. Stroke volume was not significantly different between non-EPC and EPC groups although EPC treatment alleviated intimal hyperplasia 28 days after intimal damage. Vascular endothelial growth factor (VEGF) and eNOS expression were significantly higher in the EPC-treated group than in the non-EPC group 3 days after intimal damage. In addition, MMP9 and 4HNE expression in the EPC-treated group was significantly lower than in the non-EPC group. Ultimately, this study found that venous transplantation of hCB-EPCs could inhibit neointimal hyperplasia, alleviate endothelial dysfunction, suppress intimal inflammation, and reduce oxidative stress during healing of intimal damage.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10467372PMC
http://dx.doi.org/10.1177/09636897231193069DOI Listing

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