ArticleExperimental and therapeutic medicine2015
Mechanisms of human amniotic epithelial cell transplantation in treating stage III pressure ulcer in a rat model.
Article in Experimental and therapeutic medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed, 3 citations in OpenAlex.
- Effects of Placenta-Derived Human Amniotic Epithelial Cells on the Wound Healing Process and TGF-β Induced Scar Formation in Murine Ischemic-Reperfusion Injury Model.Stem cell reviews and reports · 2022Article
- Characteristics and Therapeutic Potential of Human Amnion-Derived Stem Cells.International journal of molecular sciences · 2021Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of the present study was to determine the function of human amniotic epithelial cell transplantation (hAECT) in promoting the healing of rats with stage III pressure ulcer (PU) and to initially investigate its possible mechanisms. A total of 96 Sprague Dawley rats were allocated at random into the model, hAECT, conventional treatment or control groups (n=24 per group). In each group, 6 rats were observed to determine the wound-healing rate. The mRNA and protein expression levels of vascular endothelial growth factor (VEGF) and tumor necrosis factor (TNF)-α in the wound tissue and serum were detected using reverse transcription-quantitative polymerase chain reaction analysis and enzyme-linked immunosorbent assay. The transplantation of hAECs significantly increased the healing rate of the stage III PUs and was accompanied by the significant upregulation of VEGF mRNA and protein expression levels and the significant downregulation of TNF-α mRNA and protein expression. Immunofluorescence staining showed that, on day 7 of transplantation, hAECs remained alive inside the skin tissues. Therefore, hAECT through subcutaneous injection appears to significantly improve the wound-healing rate of stage III PUs in rats, and this effect may be associated with the upregulation of the proangiogenic factor VEGF and the downregulation of the inflammatory cytokine TNF-α.
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