| First Author | Han YH | Year | 2020 |
| Journal | In Vivo | Volume | 34 |
| Issue | 1 | Pages | 133-141 |
| PubMed ID | 31882472 | Mgi Jnum | J:295008 |
| Mgi Id | MGI:6459307 | Doi | 10.21873/invivo.11754 |
| Citation | Han YH, et al. (2020) Deletion of Peroxiredoxin II Inhibits the Growth of Mouse Primary Mesenchymal Stem Cells Through Induction of the G0/G1 Cell-cycle Arrest and Activation of AKT/GSK3beta/beta-Catenin Signaling. In Vivo 34(1):133-141 |
| abstractText | BACKGROUND/AIM: Dermal mesenchymal stem cells (DMSCs) are pluripotent stem cells found in the skin which maintain the thickness of the dermal layer and participate in skin wound healing. MATERIALS AND METHODS: The MTT assay was performed to detect cell proliferation and cell-cycle progression and cell-surface markers were assessed by flow cytometry. The levels of proteins in related signaling pathways were detected by western blotting assay and the translocation of beta-catenin into the nucleus were detected by immunofluorescence. Red oil O staining was performed to examine the differentiational ability of DMSCs. RESULTS: Knockout of PRDX2 inhibited DMSC cell growth, and cell-cycle arrest at G0/G1 phase; p16, p21 and cyclin D1 expression levels in Prdx2 knockout DMSCs were significantly increased. Furthermore, AKT phosphorylation were significantly increased in Prdx2 knockout DMSCs, GSK3beta activity were inhibited, result in beta-Catenin accumulated in the nucleus. CONCLUSION: In conclusion, these results demonstrated that PRDX2 plays a pivotal role in regulating the proliferation of DMSCs, and this is closely related to the AKT/glycogen synthase kinase 3 beta/beta-catenin signaling pathway. |
