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. 2010 Mar 10;30(10):1742–1755. doi: 10.1038/jcbfm.2010.36

Figure 6.

Figure 6

E2 decreases BCRP transport activity through nongenomic signaling. (A) One hour exposure of brain capillaries to E2 does not affect BCRP monomer or dimer protein expression. β-Actin was used as protein loading control. (B) Lactacystin, a proteasome inhibitor, does not block E2-mediated reduction of BODIPY FL prazosin fluorescence in capillary lumens, indicating that proteasomal degradation is not involved in BCRP downregulation caused by E2. Inhibition of transcription with actinomycin D (C) and inhibition of translation with cycloheximide (D) did not reverse BCRP downregulation by E2. This indicates that E2-mediated downregulation of BCRP is independent of transcription and translation. For B, C, and D, FTC was used as a positive control for BCRP inhibition. Each data point represents the mean±s.e.m. for 10 to 15 brain capillaries from a single preparation (pooled tissue from 10 rats). Units are arbitrary fluorescence units (scale 0 to 255). Statistical comparison: ***significantly lower than controls, P<0.001. BCRP, breast cancer resistance protein; FTC, fumitremorgin C.