Knockdown of miR-23, miR-27, and miR-24 alters fetal liver development and blocks fibrosis in mice
Open accessAbstract
MicroRNAs (miRNAs) regulate cell fate selection and cellular differentiation. miRNAs of the miR23b polycistron (miR-23b, miR-27b, and miR-24) target components of the TGF-β signaling pathway and affect murine bile ductular and hepatocyte cell fate selection in vitro. Here we show that miR-23b polycistron miRNAs directly target murine Smad4, which is required for TGF-β signaling. Injection of antagomirs against these miRNAs directly into E16.5 murine fetuses caused increased cytokeratin expression in sinusoids and primitive ductular elements throughout the parenchyma of newborn mice. Similar antagomir injection in newborn mice increased bile ductular differentiation in the liver periphery and reduced hepatocyte proliferation. Antagomir injection in newborn Alb/TGF-β1 transgenic mice that develop fibrosis inhibited the development of fibrosis, and injection of older mice caused the resolution of existing fibrosis. Furthermore, murine stellate cell activation, including ColA1 and ACTA2 expression, is regulated by miR-23b cluster miRNAs. In summary, knockdown of miR-23b cluster miRNAs in fetal and newborn liver promotes bile duct differentiation and can block or revert TGF-β-induced liver fibrosis that is dependent on stellate cell activation. These data may find practical application in the highly needed development of therapies for the treatment of fibrosis.
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Functional studies in mice identified the miR-23 functional cluster as a regulator of liver fibrosis.
“The functional studies in mice of different ages have identified the miR-23 functional cluster as a regulator of liver fibrosis.”
From Recent advances of miR-23 in human diseases and growth development (2025) · cites this paper as [17]
Direct injection of exogenous miR-23-27-24 cluster-specific inhibitor (antagomirs) into neonatal mice promoted bile duct differentiation and reduced hepatocyte proliferation.
“direct injection of exogenous miR-23-27-24 cluster-specific inhibitor (named antagomirs) into neonatal mice promoted bile duct differentiation and reduced hepatocyte proliferation.”
From Recent advances of miR-23 in human diseases and growth development (2025) · cites this paper as [17]
Antagomirs can inhibit fibrosis development in newborn Alb/TGF-β1 transgenic mice, while injection in old mice restored existing fibrosis.
“Antagomirs can inhibit fibrosis development in newborn Alb/TGF-β1 transgenic mice, while injection in old mice restored the existing fibrosis [17].”
From Recent advances of miR-23 in human diseases and growth development (2025) · cites this paper as [17]
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- Authors
- Rogler, C. E., Matarlo, J. S., Kosmyna, B., Fulop, D., & Rogler, L. E.
- Affiliations
- Albert Einstein College of Medicine (US)
- Venue
- Gene Expression
- Publisher
- Xia & He Publishing
- Published
- 2017-02-10
- Volume
- 17
- Issue
- 2
- Pages
- 99-114
- ISSN
- 1052-2166 (ISSN-L)
- PMC
- PMC8751183
- OpenAlex
- W2563094638
- Cited by
- 23
- References
- 54
- Citations by year
- 2026: 1 · 2024: 3 · 2023: 3 · 2022: 2 · 2021: 3 · 2020: 2 · 2019: 2 · 2018: 6 · 2017: 1
- FWCI
- 2.17
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Gene Expression (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Cancer Institute (R01CA037232)
- National Institute of Diabetes and Digestive and Kidney Diseases (P30DK041296)
- Topics
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
- Keywords
- miR-23b, miR-27b, miR-24, fetal liver development, liver fibrosis, TGF-beta signaling, SMAD4, hepatocyte proliferation, stellate cell activation, cytokeratin, hepatocyte differentiation
- MeSH terms
- Actins, Animals, Bile Ducts, Cell Differentiation, Cell Line, Liver, Liver Cirrhosis, Mice, Inbred C57BL, Mice, Transgenic, Hepatocytes, MicroRNAs, Organogenesis, Fetal Development, Cell Proliferation, Mice, Transforming Growth Factor beta1, Hepatic Stellate Cells
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