Purpose: Use FOXO3A knockout mice to explore the effect of FOXO3A on ionizing radiation (IR) damage in the hematopoietic system.
Method: FOXO3A-/- mice and WT mice (FVB/N) were divided into wild-type mouse control group (WT group), FOXO3A-/- mouse control group (FOXO3A-/- group), wild-type mouse Irradiation group (WT+IR), FOXO3A-/- mouse irradiation group (FOXO3A-/-+IR) four groups, respectively received fake irradiation and 4 Gy X-ray total body irradiation (total bod yirradiation, TBI), the dose rate was 0.9Gy /min. 14 days after receiving TBI, FOXO3A-/- mice and WT mice were tested for organ index, peripheral blood and bone marrow cell count, bone marrow cell typing, hematopoietic progenitor cells (HPCs), granulocyte macrophage colony forming units (colony Forming unit-granulocyte and macrophage, CFU-GM) formation ability, observe the effect of FOXO3A gene knockout on radiation damage of hematopoietic system.
Results: Under physiological conditions, the count of bone marrow nucleated cells in FOXO3A-/- mice decreased and the proportion of HPCs increased (P<0.05); 14 days after mice received 4GyX-ray TBI, FOXO3A gene knockout would aggravate ionizing radiation-induced HPCs and The proportion of hematopoietic stem cells (HSCs) decreases, but it also inhibits the decrease in the number of bone marrow nucleated cells induced by radiation and the decrease in the ability of hematopoietic progenitor cells to form CFU-GM.
Conclusion: FOXO3A gene knockout disrupts the homeostasis of the hematopoietic system, aggravates the radiation damage of HPCs and HSCs in TBI mice, and has a certain impact on the radiation sensitivity of hematopoietic cells. FOXO3A's regulatory role in the hematopoietic system ionizing radiation damage and whether it can be The target for prevention and treatment of damage remains to be further studied.