Knockout of E2F1 Inhibits Adipose Stem Cell Proliferation and Differentiation in Fat Transplantation by Repressing Peroxisome Proliferator-Activated Receptor Gamma Expression.

Abstract Adipose-derived stem cells (ADSCs) possess pluripotent differentiation potential and self-replication ability, which is highly significant in the field of tissue engineering. Cell-assisted lipotransfer (CAL) with ADSCs benefits fat survival. In this study, we focus on the effect of transcription factor E2F1 during CAL. The wild-type (WT) ADSCs were mixed with WT adipocytes, and the E2F1–/– ADSCs were mixed with E2F1–/– adipocytes. Then 2 cell mixtures were inoculated on the back 2 sides of E2F1–/– mice, respectively denoted as the WT group (WT ADSCs + WT adipose cells) and E2F1–/– group (E2F1–/– ADSCs + E2F1–/– adipose cells). At week 4, the fat graft was heavier in the WT group, with less necrotic area, more survival of mature adipocytes, and more proliferating ADSCs, compared with the E2F1–/– group. More capillaries were transformed from ADSCs in the WT group than in the E2F1–/– group. The in vitro protein levels of peroxisome proliferator–activated receptor gamma (PPAR-γ) were higher in WT ADSCs than in E2F1–/– ADSCs. Therefore, these findings suggest that knockout of E2F1 could affect ADSCs to inhibit the survival of fat grafts by downregulating PPAR-γ expression.