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/GSK3β/β-Catenin Signaling

• Published in: In vivo (Athens) 2020, Vol.34 (1), p.133-141
• Main Authors: Han, Ying-Hao, Jin, Mei-Hua, Jin, Ying-Hua, Yu, Nan-Nan, Liu, Jun, Zhang, Yong-Qing, Cui, Yu-Dong, Wang, Ai-Guo, Lee, Dong-Seok, Kim, Sun-Uk, Kim, Ji-Su, Kwon, Taeho, Sun, Hu-Nan
• Format: Article
• Language: English
• ISSN: 0258-851X; 1791-7549
• DOI: 10.21873/invivo.11754

BACKGROUND/AIMDermal 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 METHODSThe 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 β-catenin into the nucleus were detected by immunofluorescence. Red oil O staining was performed to examine the differentiational ability of DMSCs. RESULTSKnockout 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, GSK3β activity were inhibited, result in β-Catenin accumulated in the nucleus. CONCLUSIONIn 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/β-catenin signaling pathway.