Fig. 7: Expandable G-heporgs recapitulated copper-stimulated ATP7B translocation. | Cell Death & Disease

Fig. 7: Expandable G-heporgs recapitulated copper-stimulated ATP7B translocation.

From: Generation of proliferative hESC-derived grape-clustered hepatocyte organoids with multipolar architecture as regenerative counterpart via synergy of YAP and IGF2 pathways

Fig. 7: Expandable G-heporgs recapitulated copper-stimulated ATP7B translocation.

A Immunofluorescence staining of F-actin and MRP2 in expandable G-heporgs under the indicated conditions. Nuclei were stained with DAPI. Scale bar = 50 μm. B Representative images of CDFDA staining in expandable G-heporgs under the indicated conditions, showing canalicular bile acid transport activity. Scale bar = 50 μm. Immunostaining of ATP7B and Goligin-97 (C) ATP7B and MDR1 (D) ATP7B and ZO1 (E) ATP7B and LAMP1 (F) in BCS-treated and CuSO4-treated expandable G-heporgs. Nuclei were stained with DAPI. Scale bar = 50 μm. White arrows indicated ATP7B colocalization with or without the above markers, and yellow arrows indicated the plot quantification direction. G Fluorescence intensity profile plots along the yellow arrows showing overlapping of ATP7B and MDR1 intensity peaks in G-heporgd treated with CuSO4, but not in the BCS-control group. H The percentage values of ATP7B intensity at which MDR1 intensity was at its maximum (n = 25 cells). Results were presented as mean ± SD. Statistical significance was determined using unpaired two-tailed Student’s t-test. ***p < 0.001.

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