Abstract:
:Chronic liver injury can cause cirrhosis and impaired liver regeneration, impairing organ function. Adult livers can regenerate in response to parenchymal insults, and multiple cellular sources have been reported to contribute to this response. In this study, we modeled human chronic liver injuries, in which such responses are blunted, without genetic manipulations, and assessed potential contributions of non-parenchymal cells (NPCs) to hepatocyte regeneration. We show that NPC-derived hepatocytes replenish a large fraction of the liver parenchyma following severe injuries induced by long-term thioacetamide (TAA) or 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) treatment. Through lineage tracing of biliary epithelial cells (BECs), we show that BECs are a source of new hepatocytes and gain an Hnf4α+CK19+ bi-phenotypic state in periportal regions and fibrotic septa. Bi-phenotypic cells were also detected in cirrhotic human livers. Together, these data provide further support for hepatocyte regeneration from BECs without genetic interventions and show their cellular plasticity during severe liver injury.
journal_name
Cell Stem Celljournal_title
Cell stem cellauthors
Deng X,Zhang X,Li W,Feng RX,Li L,Yi GR,Zhang XN,Yin C,Yu HY,Zhang JP,Lu B,Hui L,Xie WFdoi
10.1016/j.stem.2018.05.022subject
Has Abstractpub_date
2018-07-05 00:00:00pages
114-122.e3issue
1eissn
1934-5909issn
1875-9777pii
S1934-5909(18)30240-6journal_volume
23pub_type
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