Alternative splicing rewires Hippo signaling pathway in hepatocytes to promote liver regeneration
Open accessAbstract
During liver regeneration, most new hepatocytes arise via self-duplication; yet, the underlying mechanisms that drive hepatocyte proliferation following injury remain poorly defined. By combining high-resolution transcriptome and polysome profiling of hepatocytes purified from quiescent and toxin-injured mouse livers, we uncover pervasive alterations in messenger RNA translation of metabolic and RNA-processing factors, which modulate the protein levels of a set of splicing regulators. Specifically, downregulation of the splicing regulator ESRP2 activates a neonatal alternative splicing program that rewires the Hippo signaling pathway in regenerating hepatocytes. We show that production of neonatal splice isoforms attenuates Hippo signaling, enables greater transcriptional activation of downstream target genes, and facilitates liver regeneration. We further demonstrate that ESRP2 deletion in mice causes excessive hepatocyte proliferation upon injury, whereas forced expression of ESRP2 inhibits proliferation by suppressing the expression of neonatal Hippo pathway isoforms. Thus, our findings reveal an alternative splicing axis that supports regeneration following chronic liver injury.
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Several studies suggest that hepatocyte proliferation leads to metabolic remodelling and that hepatocytes across the liver can adapt dynamically to changes during regeneration.
“Several studies suggest that hepatocyte proliferation leads to metabolic remodelling and that hepatocytes across the liver can adapt dynamically to changes during regeneration106,107,[131], [132], [133], [134], [135]”
From Distinct hepatocyte identities in liver homeostasis and regeneration (2023) · cites this paper as [131]
The Results section, “Regenerating hepatocytes reactivate neonatal gene expression patterns” (page not provided), reports increased proliferation and reduced expression of transcripts associated with metabolic processes in toxin-injured mouse hepatocytes. It describes these changes as responses to injury, not evidence that proliferation causes metabolic remodelling. The cited passages also do not establish that hepatocytes across the liver adapt dynamically. (LLM, conf=0.83)
Experimental — accuracy not yet measuredFollowing injury, ESRP2 activity is transiently suppressed to activate a fetal splicing program, which attenuates Hippo signaling and facilitates liver regeneration.
“Following injury, ESRP2 activity is transiently suppressed to activate a fetal splicing program, which attenuates Hippo signaling and facilitates liver regeneration (Bangru et al. 2018).”
From ESRP2–microRNA-122 axis promotes the postnatal onset of liver polyploidization and maturation (2025) · cites this paper as Bangru et al. 2018
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- Authors
- Bangru, S., Arif, W., Seimetz, J., Bhate, A., Chen, J., Rashan, E. H., Carstens, R. P., Anakk, S., & Kalsotra, A.
- Affiliations
- University of Illinois Urbana-Champaign (US)
- University of Pennsylvania (US)
- Corresponding author
- Kalsotra, Auinash
- ORCID
- Venue
- Nature Structural & Molecular Biology
- Published
- 2018-09-24
- Volume
- 25
- Issue
- 10
- Pages
- 928-939
- ISSN
- 1545-9985 (ISSN-L)
- 1545-9993
- PMC
- PMC6173981
- OpenAlex
- W2890730711
- Cited by
- 85
- References
- 76
- Citations by year
- 2026: 3 · 2025: 12 · 2024: 16 · 2023: 13 · 2022: 12 · 2021: 13 · 2020: 12 · 2019: 2 · 2018: 2
- FWCI
- 4.54
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Structural & Molecular Biology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- American Heart Association
- Nature
- National Institutes of Health
- National Heart, Lung, and Blood Institute (R01HL126845)
- National Institute of General Medical Sciences (T32GM070421)
- National Institute of Allergy and Infectious Diseases (R01AI081710)
- National Institute of Diabetes and Digestive and Kidney Diseases (F30DK108567, R01DK113080)
- Topics
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA Research and Splicing
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Hippo pathway signaling and YAP/TAZ
- Keywords
- alternative splicing, Hippo signaling pathway, liver regeneration, hepatocyte proliferation, ESRP2, splicing regulators, mRNA translation, polysome profiling, chronic liver injury
- MeSH terms
- Hippo Signaling Pathway, Animals, Gene Expression Regulation, Liver Regeneration, RNA, Messenger, Signal Transduction, RNA-Binding Proteins, Protein Serine-Threonine Kinases, Alternative Splicing, Gene Expression Profiling, Hepatocytes, Cell Proliferation, Mice
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