Fig. 8.

Neutralizing interaction between VCAM-1 and VLA-4 reverses the defect involving regimen-induced HSPC mobilization in KO mice. a–c G-CSF-induced HSPC mobilization assays with anti-VCAM-1 Ab. n = 5 per group. a WBC counts from experimental animals until day 5 after G-CSF and Ab treatment. b Representative image of spleens (left) and absolute number of splenocytes from experimental animals on day 5 after G-CSF and Ab treatment (right). c CFU-C in the BM (femur), PB, and spleen (SP) from experimental animals on day 5 after G-CSF and Ab treatment. d, e WBC counts (d) and CFU-C (e) in PB from experimental animals 3 h after AMD3100 and Ab treatment. n = 5 per group. f–h 5-FU-induced HSPC cell mobilization assays with anti-VCAM-1 Ab. n = 5 per group. f Comparison of WBC counts between WT and KO mice at indicated time points after 5-FU and Ab treatment. g Representative image of spleen from a WT and KO mouse (left) and absolute number of splenocytes (right) of WT and KO mice on day 16 after 5-FU and Ab treatment. h CFU-C in the BM (femur), PB, and spleen (SP) of WT and KO mice on day 16 after 5-FU and Ab treatment. “−“, treatment with an isotype control Ab; “ + “, treatment with anti-VCAM-1 Ab. Statistical significance was assessed by two-tailed Student’s t-test. **P < 0.01. All data are presented as the mean ± SEM. Source data are provided as a Source Data File