Fig. 6.
Fig. 6. HA binding by mobilized blood HPCs is increased when cell metabolism, lipid rafts, or cytoskeletal assembly are inhibited. Mobilized blood HPCs from 6 different individuals were treated with sodium azide, nystatin, or cytochalasin B as indicated in Materials and Methods, followed by the addition of HA-FITC and then MoAbs to stain HPCs. The same pattern was observed for all 6 samples. The percentage of increase above basal HA binding (set as 100%) in the absence of these inhibitors was calculated as the MFI of HA binding in the treated cultures divided by that of the control cultures × 100 − 100%. For azide, the mean was 130% ± 25%; for nystatin, the mean was 18% ± 3%; and for cytochalasin B, the mean was 89% ± 15% increase above basal HA binding.**P < .01 as compared with the basal HA binding of untreated HPCs. The pattern of inhibition for all three agents was the same for all 6 patient samples analyzed.

HA binding by mobilized blood HPCs is increased when cell metabolism, lipid rafts, or cytoskeletal assembly are inhibited. Mobilized blood HPCs from 6 different individuals were treated with sodium azide, nystatin, or cytochalasin B as indicated in Materials and Methods, followed by the addition of HA-FITC and then MoAbs to stain HPCs. The same pattern was observed for all 6 samples. The percentage of increase above basal HA binding (set as 100%) in the absence of these inhibitors was calculated as the MFI of HA binding in the treated cultures divided by that of the control cultures × 100 − 100%. For azide, the mean was 130% ± 25%; for nystatin, the mean was 18% ± 3%; and for cytochalasin B, the mean was 89% ± 15% increase above basal HA binding.**P < .01 as compared with the basal HA binding of untreated HPCs. The pattern of inhibition for all three agents was the same for all 6 patient samples analyzed.

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