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Conditioned medium derived from human amniotic stem cells delays H(2)O(2)-induced premature senescence in human dermal fibroblasts

Stem cells derived from human amniotic membrane (hAM) are promising targets in regenerative medicine. A previous study focused on human amniotic stem cells in skin wound and scar-free healing. The present study aimed to investigate whether hydrogen peroxide (H(2)O(2))-induced senescence of human der...

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Detalles Bibliográficos
Autores principales: Pan, Changwei, Lang, Hongxin, Zhang, Tao, Wang, Rui, Lin, Xuewen, Shi, Ping, Zhao, Feng, Pang, Xining
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6777671/
https://www.ncbi.nlm.nih.gov/pubmed/31545472
http://dx.doi.org/10.3892/ijmm.2019.4346
Descripción
Sumario:Stem cells derived from human amniotic membrane (hAM) are promising targets in regenerative medicine. A previous study focused on human amniotic stem cells in skin wound and scar-free healing. The present study aimed to investigate whether hydrogen peroxide (H(2)O(2))-induced senescence of human dermal fibroblasts (hDFs) was influenced by the anti-aging effect of conditioned medium (CdM) derived from human amniotic stem cells. First, the biological function of two types of amniotic stem cells, namely human amniotic epithelial cells (hAECs) and human amniotic mesenchymal stem cells (hAMSCs), on hDFs was compared. The results of cell proliferation and wound healing assays showed that CdM promoted cell proliferation and migration. In addition, CdM from hAECs and hAMSCs significantly promoted proliferation of senescent hDFs induced by H(2)O(2). These results indicated that CdM protects cells from damage caused by H(2)O(2). Treatment with CdM decreased senescence-associated β-galactosidase activity and improved the entry of proliferating cells into the S phase. Simultaneously, it was found that CdM increased the activity of superoxide dismutase and catalase and decreased malondialdehyde by reducing H(2)O(2)-induced intracellular reactive oxygen species production. It was found that CdM downregulated H(2)O(2)-stimulated 8-hydroxydeoxy-guanosine and γ-H2AX levels and decreased the expression of the senescence-associated proteins p21 and p16. In conclusion, the findings indicated that the paracrine effects derived from human amniotic stem cells aided delaying oxidative stress-induced premature senescence.