Fig. 6.
Fig. 6. Two examples of rhodamine content (A and C) in AML blasts after the rhodamine efflux assay with (2) or without (1) verapamil in the efflux medium. Efflux inhibition by verapamil caused a higher cellular rhodamine content predominantly in the RhoD cells. RhoD blasts were sorted and triggered to proliferate by exposure to HGFs for 48 hours. Effective proliferation induction resulted in an increase of cellular rhodamine content (A2 and C2). In these samples, only a subpopulation of the blasts became rhodamine bright after proliferation induction. Efflux modulation by verapamil was negligible in the rhodamine bright cells. The persisting rhodamine dull cells kept their sensitivity to efflux modulation by verapamil (B2 and D2).

Two examples of rhodamine content (A and C) in AML blasts after the rhodamine efflux assay with (2) or without (1) verapamil in the efflux medium. Efflux inhibition by verapamil caused a higher cellular rhodamine content predominantly in the RhoD cells. RhoD blasts were sorted and triggered to proliferate by exposure to HGFs for 48 hours. Effective proliferation induction resulted in an increase of cellular rhodamine content (A2 and C2). In these samples, only a subpopulation of the blasts became rhodamine bright after proliferation induction. Efflux modulation by verapamil was negligible in the rhodamine bright cells. The persisting rhodamine dull cells kept their sensitivity to efflux modulation by verapamil (B2 and D2).

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