American Society of Hematology

Fig. 1.

$Fig. 1. Deficiency or inhibition of endothelial selectins increase circulating hematopoietic progenitors. / (A), The low-density fraction of blood cells from wild-type and P- and E-selectin-deficient mice was isolated and plated to assay colony-forming units in culture (CFU-Cs). Colonies were scored using an inverted microscope after 7 days in culture. n = 4-5; *P < .05 compared with wild-type. (B), Wild-type (WT) and E-selectin-deficient (E−/−) mice were injected intravenously with either anti-P-selectin antibody or isotype-matched IgG control (1 mg/kg) for 3 consecutive days. Twenty-four hours after the last dose, low-density blood cells were isolated and assayed for CFU-C content. n = 3-4; # P < .05 compared with the other groups.$

Deficiency or inhibition of endothelial selectins increase circulating hematopoietic progenitors.

(A), The low-density fraction of blood cells from wild-type and P- and E-selectin-deficient mice was isolated and plated to assay colony-forming units in culture (CFU-Cs). Colonies were scored using an inverted microscope after 7 days in culture. n = 4-5; *P < .05 compared with wild-type. (B), Wild-type (WT) and E-selectin-deficient (E−/−) mice were injected intravenously with either anti-P-selectin antibody or isotype-matched IgG control (1 mg/kg) for 3 consecutive days. Twenty-four hours after the last dose, low-density blood cells were isolated and assayed for CFU-C content. n = 3-4; # P < .05 compared with the other groups.

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