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Akbari, Soheil; Sevinç, Gülben Gürhan; Ersoy, Nevin; Basak, Onur; Kaplan, Kubra; Sevinç, Kenan; Ozel, Erkin; Sengun, Berke; Enustun, Eray; Ozcimen, Burcu; Bagriyanik, Alper; Arslan, Nur; Önder, Tamer Tevfik; Erdal, Esra
Stem cell reports, 10/2019, Letnik: 13, Številka: 4Journal Article
Organoid technologies have become a powerful emerging tool to model liver diseases, for drug screening, and for personalized treatments. These applications are, however, limited in their capacity to generate functional hepatocytes in a reproducible and efficient manner. Here, we generated and characterized the hepatic organoid (eHEPO) culture system using human induced pluripotent stem cell (iPSC)-derived EpCAM-positive endodermal cells as an intermediate. eHEPOs can be produced within 2 weeks and expanded long term (>16 months) without any loss of differentiation capacity to mature hepatocytes. Starting from patient-specific iPSCs, we modeled citrullinemia type 1, a urea cycle disorder caused by mutations in the argininosuccinate synthetase (ASS1) enzyme. The disease-related ammonia accumulation phenotype in eHEPOs could be reversed by the overexpression of the wild-type ASS1 gene, which also indicated that this model is amenable to genetic manipulation. Thus, eHEPOs are excellent unlimited cell sources to generate functional hepatic organoids in a fast and efficient manner. Display omitted •iPSC-derived EpCAM+ endodermal cells generate functional hepatic organoids (eHEPOs)•eHEPOs can be stably maintained in long-term culture•An organoid-based model for a urea cycle disorder (citrullinemia) is generated•Genetic manipulation of disease-specific eHEPOs rescues disease phenotype Erdal and colleagues generated a hepatic organoid (eHEPO) culture system using human iPSC-derived EpCAM-positive endodermal cells. eHEPOs can be produced within 2 weeks and expanded long term (>16 months) without any loss of differentiation capacity to mature hepatocytes. Starting from patient-specific iPSCs, a urea cycle disorder, citrullinemia, was modeled and disease phenotype was rescued via overexpression of wild-type ASS1 gene.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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in: SICRIS
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