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. Author manuscript; available in PMC: 2016 Dec 16.
Published in final edited form as: Cell Rep. 2016 Dec 6;17(10):2584–2595. doi: 10.1016/j.celrep.2016.11.031

Figure 5. HSCs from chronically infected animals have increased stress but no increase in rate of apoptosis.

Figure 5

(A) Ki67+ HSCs shown as % of total HSCs (LK CD150+ CD48− CD34−) in naïve, 1 month or 3 month M. avium-infected mice. Data represent 2 independent experiments, with n=6–10 per group. (B) ROS levels in HSCs of naïve and 4 week M. avium infected mice shown as a mean fluorescent intensity (MFI) of CellRox staining. TBHP was the positive control. Data represent 2 independent experiments, n=6–8 per group. (C) DNA damage was assessed using phospho-Kap1 (pKap1) staining of HSCs from naïve or M. avium-infected mice. UV-treated cells were used as positive control. Data are representative of 2 independent studies, n=3–5 per group. (D) % of HSCs with γH2AX staining. Numbers above the bars refer to n for each condition. 1Gy irradiation was used as a positive control. Data are representative of 2 independent experiments. (E–F) Caspase 3/7 activity in 400 HSCs after 12hrs of in vitro culture. (E) HSCs from 1 month or 3 month infected mice. (F) HSCs from control or 24hr IFNγ-treated mice. (G) Caspase 3/7 activity immediately after isolation of 400 HSCs from naïve or M. avium-infected mice. Results for E–G are representative of 2–5 independent experiments, n=3 per group. Data are presented as mean ± SEM; * p<0.05, ** p<0.01, *** p<0.001, n.s. not significant. See also Figure S5.