Cxcl12 deficiency leads to hematopoietic progenitor pool expansion in BM. (A) 12 weeks (wks) after tamoxifen treatment, there was no significant change of the total number of BM nucleated cells between Cxcl12-WT (n = 10) and Cxcl12-cKO mice (n = 11) (mean ± SEM; P = .812). (B-C) Representative figures of the gating of Lin⁻Sca-1⁺c-Kit⁺ (LSK) cell populations in BM (B) or peripheral blood mononuclear cells (PBMCs) (C) of Cxcl12-WT and Cxcl12-cKO mice 2 wks or 12 wks after tamoxifen treatment. Right panel shows the percentage of LSK cells in BM or PB (mean ± SEM; *P < .05, **P < .005; n = 6 each). (D) Statistical bar graphs of colony forming unit cell (CFU-C) assay of BM and PB derived from Cxcl12-WT and Cxcl12-cKO mice 2 and 12 wks after tamoxifen treatment (means ± SEM; *P < .05, **P < .005, ***P < .001; n = 6 each group). (E) Lineage-specific marker analysis for BM cells from Cxcl12-WT and Cxcl12-cKO mice 12 wks after tamoxifen treatment. Data are expressed as mean ± SEM (***P < .001; n = 3). (F) Spleen cellularity, spleen/body weight ratio, spleen LSK cells, and CFU-C counts in spleen were examined 12 wks after tamoxifen treatment (mean ± SEM; *P < .05; for spleen cellularity and spleen/body weight ratio n = 10 each, for LSK and CFU-C n = 4 each). For all bar graphs, black bars are Cxcl12-WT and gray bars are Cxcl12-cKO.