Fig. 6: ME7 infection-related impairment of BM renders HSCs senescent.
A Schematic diagram of the transplantation experiment to determine whether HSC senescence in ME7-infected mice was due to ME7-mediated preferential impairment of the BM microenvironment. Normal BM cells (2 × 106, CD45.1) from Prnp+/+ (WT) or Prnp−/− (KO) mice were non-competitively transplanted into control or ME7-infected mice that had received sub-lethal irradiation at 3 months post-infection (CD45.2, 500 rads, n = 5). B The CD45.1/CD45.2 ratio in PB of recipient mice at 4 months post-transplantation was evaluated by flow cytometry (n = 5). Percentage (C, n = 5), mitochondrial ROS level (D, n = 5), SA-β-gal activity (E, n = 5), and p16 expression level (F, n = 5) of donor cell-derived HSCs were analyzed in the BM of transplanted recipient mice. All data are presented as means ± SDs. *p < 0.05, **p < 0.01, and ***p < 0.001 vs. control, as determined by Student’s t test.
