Role of p53 and intrinsic apoptosis pathway in IFN-1–exposed HSCs. (A) Experimental design for HSC apoptosis and gene expression assays. (B) CC3 levels in WT, Trp53^−/−, and BakBax^cKO HSCs treated for 12 h ± 100 ng/ml IFN-α (n = 3–4). Results are expressed as fold change relative to IFN-α control HSCs. (C and D) Quantitative RT-PCR analyses for Bcl2 family gene expression in (C) WT and (D) Ctrl and Trp53^−/− HSCs treated for 12 h ± 100 ng/ml IFN-α (n = 3–4). Results are expressed as log₂ fold expression relative to IFN-α controls. (E) Experimental design for in vivo BrdU incorporation analyses in HSCs from poly I:C–treated Ctrl, Trp53^−/−, Foxo3a^−/− mice. (F) Mean levels of BrdU incorporation in Trp53^−/− (left) and Foxo3a^−/− (right) mice compared with their respective Ctrl mice (3 mice/group). (G) Model for the role of p53 in IFN-1–exposed HSCs. All data are mean ± SD; statistical significance was determined by Student’s t test (*, P ≤ 0.05; **, P ≤ 0.01; ***, P ≤ 0.005).