A homeostatic Arid1a-dependent permissive chromatin state licenses hepatocyte responsiveness to liver-injury-associated YAP signaling
Open accessAbstract
Following injury, differentiated epithelial cells can serve as a stem cell-independent source for tissue regeneration by undergoing reprogramming into other cell types. The intrinsic molecular basis underlying plasticity of differentiated cells remains largely unaddressed. Here we show that Arid1a, a key component of the SWI/SNF chromatin remodeling complex, controls liver regeneration and gene expression associated with emergence of injury-induced liver-progenitor-like cells (LPLCs). Hepatocyte-specific Arid1a ablation reduces LPLC gene expression in several models of periportal liver injury and impairs liver regeneration, leading to organ dysfunction. Arid1a establishes a permissive chromatin state at LPLC-enriched genes during homeostasis, suggesting it endows hepatocytes with competence to respond to injury-induced signals. Consistently, Arid1a facilitates binding of YAP, a critical regeneration signaling pathway, to LPLC-enriched genes, and Arid1a deletion prevents their YAP-associated induction following injury. Together, these findings provide a framework for studying the contributions of injury-induced LPLCs to periportal liver regeneration.
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Cholestatic injury activates YAP signalling and thereby reprogrammes periportal hepatocytes, reducing the amount of metabolically active workers in this zone.
“Such cholestatic injury also activates YAP signalling and thereby reprogrammes periportal hepatocytes, reducing the amount of metabolically active workers in this zone.57,94,102”
From Distinct hepatocyte identities in liver homeostasis and regeneration (2023) · cites this paper as [102]
The Introduction and the section on Arid1a-dependent YAP activation describe periportal injury, YAP-responsive hepatocytes, and their conversion into liver-progenitor-like cells. The DDC-injury results also show that some hepatocyte-derived cells acquire ductal-like features and diminish expression of the mature hepatocyte gene Fah. The paper does not establish a reduction in the number of metabolically active hepatocytes in the periportal zone, so that consequence goes beyond its findings. (LLM, conf=0.83)
Experimental — accuracy not yet measuredIn 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 [8]
The section 'Arid1a Facilitates Liver-Progenitor-Like Cell Formation in Periportal Liver Injury' reports LPLC formation after periportal injury, and the figure discussion places related cells in the periportal area (page not provided). Our copy does not say that LPLCs are mainly generated one to five cell layers from injured bile ducts; searches for that distance and for 'layers' did not find it. (LLM, conf=0.85)
Experimental — accuracy not yet measuredWhen LPLC formation is restrained, injured livers show prolonged hepatocyte proliferation, enhanced biliary injury, and reduced fibrosis resolution.
“When the formation of LPLCs was restrained, injured livers showed prolonged hepatocyte proliferation, enhanced biliary injury, and reduced fibrosis resolution.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 [8]
The section on Arid1a-dependent LPLC formation and liver regeneration reports that, after eight weeks of recovery, hepatocytes continued to proliferate in Arid1a-KO mice, in which LPLC formation was impaired. It does not establish enhanced biliary injury or reduced fibrosis resolution; it says DDC-induced ductular reactions resolved in both knockout and control mice. (LLM, conf=0.89)
Experimental — accuracy not yet measuredArid1a supports hepatocyte reprogramming by facilitating binding of YAP to genes associated with a liver progenitor cell state.
“Arid1a supports hepatocyte reprogramming by facilitating binding of YAP to genes associated with a liver progenitor cell state.102”
From Distinct hepatocyte identities in liver homeostasis and regeneration (2023) · cites this paper as [102]
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 [8]
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 [8]
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 [8]
Chromatin regions of liver progenitor genes remain accessible in mature hepatocytes, endowing hepatocytes with intrinsic reprogramming competence for rapid response to extrinsic injury signals and expression of these genes.
“Our previous study has revealed that the chromatin regions of liver progenitor genes remain accessible in mature hepatocytes, thereby endowing hepatocytes with intrinsic ''reprogramming competence'' for the rapid response to extrinsic injury signals and expression of these genes.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 [8]
Genes expressed in liver progenitors remained accessible in mature hepatocytes via Arid1a regulation, endowing hepatocytes with competence to respond rapidly to reprogramming signals.
“We previously found that genes expressed in liver progenitors remained accessible in mature hepatocytes via Arid1a regulation, endowing hepatocytes with the competence to respond rapidly to reprogramming signals.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 [8]
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- Authors
- Li, W., Yang, L., He, Q., Hu, C., Zhu, L., Ma, X., Ma, X., Bao, S., Li, L., Chen, Y., Deng, X., Zhang, X., Cen, J., Zhang, L., Wang, Z., Xie, W.-F., Li, H., Li, Y., & Hui, L.
- Affiliations
- Chinese Academy of Sciences (CN)
- Shanghai Institute of Nutrition and Health (CN)
- Second Military Medical University (CN)
- University of Michigan (US)
- Shanghai Jiao Tong University (CN)
- Corresponding author
- Li, Hong
- Li, Yixue
- Hui, Lijian
- ORCID
- Venue
- Cell Stem Cell
- Publisher
- Elsevier BV
- Published
- 2019-07
- Volume
- 25
- Issue
- 1
- Pages
- 54-68.e5
- ISSN
- 1875-9777 (ISSN-L)
- 1934-5909
- OpenAlex
- W2954700532
- Cited by
- 124
- References
- 67
- Citations by year
- 2026: 10 · 2025: 16 · 2024: 19 · 2023: 24 · 2022: 19 · 2021: 20 · 2020: 14 · 2019: 2
- FWCI
- 8.77
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell stem cell (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Science and Technology Commission of Shanghai Municipality
- National Natural Science Foundation of China
- National Major Science and Technology Projects of China
- Chinese Academy of Sciences
- Topics
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Hippo pathway signaling and YAP/TAZ
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Congenital heart defects research
- Keywords
- ARID1A, SWI/SNF complex, YAP signaling, liver regeneration, chromatin state, tissue regeneration
- MeSH terms
- Cell Self Renewal, YAP-Signaling Proteins, Animals, Chromatin, DNA-Binding Proteins, Homeostasis, Liver Regeneration, Mice, Transgenic, Transcription Factors, Signal Transduction, Cell Cycle Proteins, Hepatocytes, Chromatin Assembly and Disassembly, Adaptor Proteins, Signal Transducing, Mice, Acute Lung Injury, Induced Pluripotent Stem Cells, Clustered Regularly Interspaced Short Palindromic Repeats
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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