Pregnane X receptor regulates liver size and liver cell fate by yes-associated protein activation in mice
Open accessAbstract
Activation of pregnane X receptor (PXR), a nuclear receptor that controls xenobiotic and endobiotic metabolism, is known to induce liver enlargement, but the molecular signals and cell types responding to PXR‐induced hepatomegaly remain unknown. In this study, the effect of PXR activation on liver enlargement and cell change was evaluated in several strains of genetically modified mice and animal models. Lineage labeling using AAV‐Tbg‐Cre‐treated Rosa26 EYFP mice or Sox9‐Cre ERT, Rosa26 EYFP mice was performed and Pxr‐null mice or AAV Yap short hairpin RNA (shRNA)‐treated mice were used to confirm the role of PXR or yes‐associated protein (YAP). Treatment with selective PXR activators induced liver enlargement and accelerated regeneration in wild‐type (WT) and PXR‐humanized mice, but not in Pxr‐null mice, by increase of cell size, induction of a regenerative hybrid hepatocyte (HybHP) reprogramming, and promotion of hepatocyte and HybHP proliferation. Mechanistically, PXR interacted with YAP and PXR activation induced nuclear translocation of YAP. Blockade of YAP abolished PXR‐induced liver enlargement in mice. Conclusion : These findings revealed a function of PXR in enlarging liver size and changing liver cell fate by activation of the YAP signaling pathway. These results have implications for understanding the physiological functions of PXR and suggest the potential for manipulation of liver size and liver cell fate.
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PXR can accelerate regeneration.
“PXR can accelerate regeneration,57, 58, 59”
From Constitutive Androstane Receptor Regulates Bile Acid Homeostasis and Metabolism During Liver Regeneration (2026) · cites this paper as [58]
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Self-citationClinical translation of liver regeneration therapies: A conceptual road map
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Helix 12 stabilization contributes to basal transcriptional activity of PXR
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Generation and network analysis of an RNA-seq transcriptional atlas for the rat
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Pregnane X receptor in drug-induced liver injury: Friend or foe?
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Self-citationRegulation of hepatic xenosensor function by HNF4alpha
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Self-citationDysregulation of intercellular signaling by MOF deletion leads to liver injury
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Self-citationThe reversal of PXR or PPARα activation-induced hepatomegaly
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Self-citationPXR activation ameliorates hyperuricemic nephropathy via NRF2 signaling
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Self-citationHNF4α improves hepatocyte regeneration by upregulating PXR
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Fenofibrate induces liver enlargement in aging mice via activating the PPARα-YAP signaling pathway
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Self-citationChronic Treatment With WY-14643 Induces Tumorigenesis and Triglyceride Accumulation in Mouse Livers
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AHR regulates liver enlargement and regeneration through the YAP signaling pathway
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Pregnane X receptor in disease: From xenobiotic sensor to therapeutic target
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Self-citationHarnessing the UDP-G/P2Y14R axis to promote liver regeneration in acute liver failure
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Self-citationThe emerging role of the Hippo signaling pathway in interorgan crosstalk
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Self-citationIs This the Time to Reconsider the Names for Xenobiotic Nuclear Receptors?
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Special Section On Drug Metabolism in Liver Injury and Repair—Editorial
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Yes-associated protein at the intersection of liver cell fate determination
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18β-glycyrrhetinic acid accelerates liver regeneration after partial hepatectomy in mice
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- Authors
- Jiang, Y., Feng, D., Ma, X., Fan, S., Gao, Y., Fu, K., Wang, Y., Sun, J., Yao, X., Liu, C., Zhang, H., Xu, L., Liu, A., Gonzalez, F. J., Yang, Y., Gao, B., Huang, M., & Bi, H.
- Affiliations
- Sun Yat-sen University (CN)
- National Institutes of Health (US)
- University of Pittsburgh (US)
- Ningbo University (CN)
- Harvard University (US)
- Corresponding author
- Bi, Huichang
- ORCID
- Venue
- Hepatology
- Published
- 2018-12-17
- Volume
- 69
- Issue
- 1
- Pages
- 343-358
- ISSN
- 0270-9139 (ISSN-L)
- 1527-3350
- PMC
- PMC6324985
- OpenAlex
- W2883896404
- Cited by
- 103
- References
- 50
- Citations by year
- 2026: 9 · 2025: 12 · 2024: 15 · 2023: 10 · 2022: 19 · 2021: 12 · 2020: 16 · 2019: 7 · 2018: 3
- FWCI
- 5.95
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- Locations
- Hepatology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- OSTI OAI (U.S. Department of Energy Office of Scientific and Technical Information) (submittedVersion)
- Funders
- National Natural Science Foundation of China (81320108027), 81573489, 81730103, B16047, 81522047)
- Natural Science Foundation of Guangdong Province (2015A030313124, 2017A030311018)
- Higher Education Discipline Innovation Project (B16047)
- Guangdong Provincial Key Laboratory of Construction Foundation (2017B030314030)
- National Institutes of Health
- National Key Research and Development Program of China (2017YFE 0109900, 2017YFC0909303, 2011A060901014)
- National Institute on Alcohol Abuse and Alcoholism (Z01AA000368)
- National Cancer Institute (R01CA222571)
- Research and Development (2011A060901014)
- 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 › Peroxisome Proliferator-Activated Receptors
- Keywords
- pregnane X receptor, YAP, hepatomegaly, hepatocyte proliferation, hepatocyte reprogramming, nuclear translocation, nuclear receptor signaling
- MeSH terms
- Pregnane X Receptor, YAP-Signaling Proteins, Animals, Cell Differentiation, Liver, Male, Mice, Inbred C57BL, Organ Size, Mice, Knockout, Cell Cycle Proteins, Hepatocytes, Adaptor Proteins, Signal Transducing, Mice
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