Bipotential Adult Liver Progenitors Are Derived from Chronically Injured Mature Hepatocytes
Open accessAbstract
Adult liver progenitor cells are biliary-like epithelial cells that emerge only under injury conditions in the periportal region of the liver. They exhibit phenotypes of both hepatocytes and bile ducts. However, their origin and their significance to injury repair remain unclear. Here, we used a chimeric lineage tracing system to demonstrate that hepatocytes contribute to the progenitor pool. RNA-sequencing, ultrastructural analysis, and in vitro progenitor assays revealed that hepatocyte-derived progenitors were distinct from their biliary-derived counterparts. In vivo lineage tracing and serial transplantation assays showed that hepatocyte-derived proliferative ducts retained a memory of their origin and differentiated back into hepatocytes upon cessation of injury. Similarly, human hepatocytes in chimeric mice also gave rise to biliary progenitors in vivo. We conclude that human and mouse hepatocytes can undergo reversible ductal metaplasia in response to injury, expand as ducts, and subsequently contribute to restoration of the hepatocyte mass.
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Following diverse injuries, often involving cholestasis, YAP signalling drives hepatocyte reprogramming via SOX9 induction.
“Following diverse injuries, often involving cholestasis, YAP signalling also drives hepatocyte reprogramming via SOX9 induction.”
From Distinct hepatocyte identities in liver homeostasis and regeneration (2023) · cites this paper as [100]
Reprogrammed zone 1 hepatocytes exhibited reduced metabolic function, upregulated tissue stem cell markers and increased proliferative capacity, contributing to regeneration.
“These reprogrammed zone 1 hepatocytes exhibited reduced metabolic function, upregulated tissue stem cell markers and increased proliferative capacity, contributing to regeneration.59,60,100,101”
From Distinct hepatocyte identities in liver homeostasis and regeneration (2023) · cites this paper as [100]
Lineage-tracing studies in animal models have confirmed that hepatocytes contribute to bile duct remodeling following cholangiocyte injury.
“Lineage-tracing studies in animal models have confirmed that hepatocytes contribute to bile duct remodeling following cholangiocyte injury10,43–48”
From HBO1 functions as an epigenetic barrier to hepatocyte plasticity and reprogramming during liver injury (2025) · cites this paper as [44]
During injury, mouse hepatocytes can be reprogrammed to proliferative biliary-like progenitor cells (HepPDs).
“Specifically, during injury, mouse hepatocytes can be reprogrammed to proliferative biliary-like progenitor cells (HepPDs) (Tarlow et al., 2014; Yanger et al., 2013”
From In Vitro Expansion of Primary Human Hepatocytes with Efficient Liver Repopulation Capacity (2018) · cites this paper as Tarlow et al., 2014
HepPDs lose hepatic features but display the characteristics of liver progenitors.
“which lose hepatic features but display the characteristics of liver progenitors (Tarlow et al., 2014”
From In Vitro Expansion of Primary Human Hepatocytes with Efficient Liver Repopulation Capacity (2018) · cites this paper as Tarlow et al., 2014
ProliHHs showed increased expression of progenitor-associated signature genes that were upregulated during conversion from human hepatocytes to HepPD cells, such as SOX9, CD133, EPCAM, CD44, CK19, and CK7.
“ProliHHs showed increased expression of progenitor-associated signature genes that were upregulated during the conversion from human hepatocytes to HepPD cells, such as SOX9, CD133, EPCAM, CD44, CK19, and CK7”
From In Vitro Expansion of Primary Human Hepatocytes with Efficient Liver Repopulation Capacity (2018) · cites this paper as Tarlow et al., 2014
In periportal injury, LPLCs are mainly generated in the region 1-5 layers away from injured bile ducts.
“In periportal injury, LPLCs are mainly generated in the region 1-5 layers away from injured bile ducts.[7][8][9]12,13”
From Kupffer-cell-derived IL-6 is repurposed for hepatocyte dedifferentiation via activating progenitor genes from injury-specific enhancers (2023) · cites this paper as [7]
In DDC-induced periportal injury, LPLCs give rise to approximately 25% of newly regenerated hepatocytes and, to some extent, cholangiocytes.
“For example, in 3,5-diethoxycarbonyl-1,4-dihydrocollidin (DDC)-induced periportal injury, LPLCs gave rise to approximately 25% of the newly regenerated hepatocytes and, to some extent, cholangiocytes.7,8”
From Kupffer-cell-derived IL-6 is repurposed for hepatocyte dedifferentiation via activating progenitor genes from injury-specific enhancers (2023) · cites this paper as [7]
Following periportal injury, hepatocytes reactivate progenitor genes and undergo dedifferentiation into liver progenitor-like cells (LPLCs) to repair the injured liver.
“Following periportal injury, hepatocytes reactivated progenitor genes and underwent dedifferentiation into liver progenitor-like cells (LPLCs) to repair the injured liver.”
From Kupffer-cell-derived IL-6 is repurposed for hepatocyte dedifferentiation via activating progenitor genes from injury-specific enhancers (2023) · cites this paper as [7]
LPLCs formed specifically around periportal regions are parenchymal cells showing hepatocyte morphology and expressing both HNF4a and SOX9.
“LPLCs, formed specifically around periportal regions, were determined as parenchymal cells both showing a hepatocyte morphology and expressing both the hepatic marker HNF4a, and the progenitor marker SOX9 (Figures 1A and 1B).[7][8][9]”
From Kupffer-cell-derived IL-6 is repurposed for hepatocyte dedifferentiation via activating progenitor genes from injury-specific enhancers (2023) · cites this paper as [7]
Mature hepatocytes were found reprogrammed into LPLCs to contribute to liver repair after periportal injury.
“Importantly, mature hepatocytes were found reprogrammed into LPLCs to contribute to liver repair after periportal injury.7,9,13”
From Kupffer-cell-derived IL-6 is repurposed for hepatocyte dedifferentiation via activating progenitor genes from injury-specific enhancers (2023) · cites this paper as [7]
Further experiments in mice have shown that hepatocytes can change into a biliary ductular phenotype and later re-differentiate into hepatocytes.
“Further experiments in mice have shown that hepatocytes can change into a biliary ductular phenotype21, 22 then later re-differentiate into hepatocytes23.”
From Hepatic progenitor cells of biliary origin with liver repopulation capacity (2015) · cites this paper as [23]
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- Authors
- Tarlow, B. D., Pelz, C., Naugler, W. E., Wakefield, L., Wilson, E. M., Finegold, M. J., & Grompe, M.
- Affiliations
- Oregon Health & Science University (US)
- Yecuris (United States) (US)
- Baylor College of Medicine (US)
- Corresponding author
- Tarlow, Branden D.
- ORCID
- Venue
- Cell Stem Cell
- Publisher
- Elsevier BV
- Published
- 2014-11
- Volume
- 15
- Issue
- 5
- Pages
- 605-618
- ISSN
- 1875-9777 (ISSN-L)
- 1934-5909
- OpenAlex
- W1968856828
- Cited by
- 533
- References
- 55
- Citations by year
- 2026: 16 · 2025: 34 · 2024: 43 · 2023: 48 · 2022: 40 · 2021: 61 · 2020: 47 · 2019: 45 · 2018: 61 · 2017: 45 · 2016: 54 · 2015: 36 · 2014: 2
- FWCI
- 25.48
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell stem cell (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Oregon Health and Science University
- National Institutes of Health (5p01dk044080-05)
- National Cancer Institute (P30CA069533)
- National Institute of General Medical Sciences (T32GM071338)
- National Institute of Diabetes and Digestive and Kidney Diseases (F30-DK09551, F30DK095514, R01DK051592, P01-DK044080, T32DK007202, P30DK056338)
- Topics
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Health Sciences › Medicine › Genetics › Mesenchymal stem cell research
- Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmacology › Drug-Induced Hepatotoxicity and Protection
- Keywords
- hepatocyte injury, liver regeneration, lineage tracing, chimeric mice, periportal zone, liver injury repair
- MeSH terms
- Animals, Cell Differentiation, Cell Separation, Clone Cells, Gene Expression Regulation, Hepatic Duct, Common, Humans, Liver, Mesoderm, Mice, Inbred C57BL, Biomarkers, Hepatocytes, Adult Stem Cells, SOX9 Transcription Factor, Cellular Microenvironment
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