Figure 2
Figure 2. dmPGE2 pulsed HSCs do not have an inherent competitive advantage in secondary transplants. (A) Schematic representation of experimental design. WBM from CD45.1 mice and CD45.2 mice was treated with both vehicle and dmPGE2 and then transplanted head to head into lethally irradiated (1100 cGy, split dose) CD45.1/CD45.2 hybrid mice as shown (2.5 × 105 cells per group). Chimerism was analyzed at 12 weeks, and bone marrow from recipients was collected and stained with fluorescent antibodies for phenotypic markers, and cells were sorted for SLAM SKL. SLAM SKL cells were transplanted head to head into a second cohort of lethally irradiated CD45.1/CD45.2 mice along with 2.0 × 105 WBM CD45.1/CD45.2 competitors, and chimerism analyzed 12 weeks later. (B) Chimerism in peripheral blood is shown for 12 weeks after the primary transplant and 12 weeks after the secondary transplant (mean ± SEM). n = 10 mice per group (total of 20 mice for primary and 20 mice for secondary); *P < .001.

dmPGE2 pulsed HSCs do not have an inherent competitive advantage in secondary transplants. (A) Schematic representation of experimental design. WBM from CD45.1 mice and CD45.2 mice was treated with both vehicle and dmPGE2 and then transplanted head to head into lethally irradiated (1100 cGy, split dose) CD45.1/CD45.2 hybrid mice as shown (2.5 × 105 cells per group). Chimerism was analyzed at 12 weeks, and bone marrow from recipients was collected and stained with fluorescent antibodies for phenotypic markers, and cells were sorted for SLAM SKL. SLAM SKL cells were transplanted head to head into a second cohort of lethally irradiated CD45.1/CD45.2 mice along with 2.0 × 105 WBM CD45.1/CD45.2 competitors, and chimerism analyzed 12 weeks later. (B) Chimerism in peripheral blood is shown for 12 weeks after the primary transplant and 12 weeks after the secondary transplant (mean ± SEM). n = 10 mice per group (total of 20 mice for primary and 20 mice for secondary); *P < .001.

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