Fig. 3.
Fig. 3. Under static conditions, adhesion of CD34+cells to BMEC monolayers is independent of E-selectin. CD34+ cells derived from CB were plated on IL-1β–activated BMEC monolayers in the presence or absence of blocking MoAb to either VCAM-1 (10 μg/mL), ICAM-1 (10 μg/mL), E-selectin (10 μg/mL), or EDTA (2 mmol/L). After incubation for 1 hour, EDTA resulted in a complete inhibition of adhesion. However, only MoAb to VCAM-1 partially blocked the adhesion of CD34+cells by 44.0% ± 5.8%, whereas MoAb to E-selectin even at high concentrations of 30 μg/mL had no effect on adhesion of CD34+ cells to endothelium. MoAb to ICAM-1 also did not have a significant effect on adhesion of CD34+ cells to BMEC (N = 4, P < .01).

Under static conditions, adhesion of CD34+cells to BMEC monolayers is independent of E-selectin. CD34+ cells derived from CB were plated on IL-1β–activated BMEC monolayers in the presence or absence of blocking MoAb to either VCAM-1 (10 μg/mL), ICAM-1 (10 μg/mL), E-selectin (10 μg/mL), or EDTA (2 mmol/L). After incubation for 1 hour, EDTA resulted in a complete inhibition of adhesion. However, only MoAb to VCAM-1 partially blocked the adhesion of CD34+cells by 44.0% ± 5.8%, whereas MoAb to E-selectin even at high concentrations of 30 μg/mL had no effect on adhesion of CD34+ cells to endothelium. MoAb to ICAM-1 also did not have a significant effect on adhesion of CD34+ cells to BMEC (N = 4, P < .01).

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