4.6 Article

Conditioned medium derived from human amniotic stem cells delays H2O2-induced premature senescence in human dermal fibroblasts

期刊

INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE
卷 44, 期 5, 页码 1629-1640

出版社

SPANDIDOS PUBL LTD
DOI: 10.3892/ijmm.2019.4346

关键词

human amniotic epithelial cells; human amniotic mesenchymal stem cells; human dermal fibroblasts; hydrogen peroxide; senescence

资金

  1. Shenyang Key R&D and Technology Transfer Program [250039]

向作者/读者索取更多资源

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 (H2O2)-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 H2O2. These results indicated that CdM protects cells from damage caused by H2O2. Treatment with CdM decreased senescence-associated beta -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 H2O2-induced intracellular reactive oxygen species production. It was found that CdM downregulated H2O2-stimulated 8-hydroxydeoxy-guanosine and gamma -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.

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