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. 2018 Aug 16;35:114–123. doi: 10.1016/j.ebiom.2018.08.014

Fig. 3.

Fig. 3

Long-term maintenance of hepatic function and HBV propagation in hiPSC liver organoids.

(A) ELISA for ALB secretion of hiPSC-HLCs and differentiated hiPSC-LOs in extended culture (n = 5, each). (B) Q-PCR analysis of CYP3A4 expression of hiPSC-LOs during extended culture, n = 3. (C) Quantification of HBV pgRNA (left) and supernatant vDNA (right) in hiPSC-HLCs (n = 4), hiPSC-LOs (n = 8), PHH-1 (n = 4) and PHH-2 (n = 4) at 10 and 20 dpi by Q-PCR. 10 dpi of hiPSC-HLCs was used as a control. (D) Immunofluorescence analysis of ALB and HBc in infected hiPSC-LOs at 10 and 20 dpi. Infection rates were calculated based on the number of HBc and ALB double positive cells (ALB+HBc+) relative to that of total ALB-positive cells (ALB+), n = 24 liver organoids. (E) Quantification of HBV pgRNA and supernatant vDNA in PXB-HH infected with supernatant of infected hiPSC-LOs (20 dpi) and HBV derived from HepG2 2.15.7 (n = 6 each) at 10 dpi, non-infected PXB-HH was used as a negative control (F) Immunofluorescence analysis of HBc in PXB-HH infected with supernatant of infected hiPSC-LOs (20 dpi) and HBV derived from HepG2 2.15.7 at 10 dpi. *p < .05, **p < .01, ***p < .001, ns, not significant.