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

08:00 EDT 20th September 2019 | BioPortfolio

Summary of "Conditioned medium derived from human amniotic stem cells delays H2O2‑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 (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 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 H2O2‑induced intracellular reactive oxygen species production. It was found that CdM downregulated H2O2‑stimulated 8‑hydroxydeoxyguanosine 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.


Journal Details

This article was published in the following journal.

Name: International journal of molecular medicine
ISSN: 1791-244X


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