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. 2014 Mar 18;9(3):e91921. doi: 10.1371/journal.pone.0091921

Figure 4. ABCB11 trafficking in control and LKB1 −/− hepatocytes.

Figure 4

(A) FRAP studies with control and LKB1 −/− mouse hepatocytes transduced with YFP-tagged ABCB11 were performed as described in detail in Figs. 2 and 3. The second phase of fluorescence recovery was markedly slower in the LKB1 −/− cells (○) as compared to control cells (•). Taurocholate (TC) accelerated the fluorescence recovery only in control hepatocytes (▪), and had no effect in LKB1 −/− cells (□). (B–C) The slopes of the second recovery phase (parameter B in the equation), which reflect initial rate of canalicular trafficking, were averaged and normalized to the untreated wild type cells. Pretreatments: TC – 100 µM taurocholate, AICAR - 500 µM AICAR, cAMP - 200 µM 8-Br-cAMP, PKAact - 50 µM 6-Bnz-cAMP, Epac - 3 µM 8-CTP-cAMP, PKAi - 500 nM PKA inhibitor. Means ± S.E.M. of at least three independent experiments are shown. Asterisks denote significant differences as compared to untreated control hepatocytes (*), to untreated LKB1 −/− cells (**), or to 8-Br-cAMP-treated cells (***), p<0.05. n.d. – not determined. Taurocholate, AICAR, and cAMP accelerated canalicular trafficking of ABCB11 in control hepatocytes. The effects were not additive. Basal level of ABCB11 trafficking to the canaliculi was reduced in the LKB1 −/− cells as compared to control cells. Taurocholate and AICAR were ineffective in these cells, however, the effect of cAMP persisted. Activation of PKA resulted in accelerated canalicular trafficking in both cell types, whereas inhibition of PKA abolished the effect of cAMP in LKB1-deficient hepatocytes.