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

Abstract

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 β-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, GSK3β activity were inhibited, result in β-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/β-catenin signaling pathway.