Figure 3
Figure 3. The most primitive LSCs from CML-CP–like mice accumulate oxidative DNA damage. (A) 8-oxoG (163 and 110 cells from 5 and 4 normal and CML-CP–like mice, respectively) and γ-H2AX (162 and 279 cells each from 4 normal and CML-CP–like mice) were detected by immunofluorescence in DAPI-counterstained nuclei of BM-derived Lin−c-Kit+Sca-1+ HSCs/LSCs from healthy (black bars) and CML-CP–like (gray bars) mice; *P < .05 in comparison with healthy counterparts. (B) 8-oxoG (left panel) and γ-H2AX (right panel) were detected in Lin−c-Kit+Sca-1+Fluor670max quiescent cells obtained from at least 5 mice per group by FACS analysis. *P ≤ .001 in comparison with healthy counterparts. DAPI, 4,6 diamidino-2-phenylindole.

The most primitive LSCs from CML-CP–like mice accumulate oxidative DNA damage. (A) 8-oxoG (163 and 110 cells from 5 and 4 normal and CML-CP–like mice, respectively) and γ-H2AX (162 and 279 cells each from 4 normal and CML-CP–like mice) were detected by immunofluorescence in DAPI-counterstained nuclei of BM-derived Linc-Kit+Sca-1+ HSCs/LSCs from healthy (black bars) and CML-CP–like (gray bars) mice; *P < .05 in comparison with healthy counterparts. (B) 8-oxoG (left panel) and γ-H2AX (right panel) were detected in Linc-Kit+Sca-1+Fluor670max quiescent cells obtained from at least 5 mice per group by FACS analysis. *P ≤ .001 in comparison with healthy counterparts. DAPI, 4,6 diamidino-2-phenylindole.

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