Mesenchymal stem cells improve liver fibrosis and protect hepatocytes by promoting microRNA-148a-5p-mediated inhibition of Notch signaling pathway
Open accessAbstract
Background: Mesenchymal stem cells (MSCs) are considered to be a potential therapeutic tool for liver fibrosis. Inhibiting the activation of hepatic stellate cells (HSCs) and protecting hepatocytes are important mechanisms for the anti-fibrotic effect of MSCs. However, how MSCs inhibit liver fibrosis by regulating the expression of microRNAs (miRNAs) has not been fully clarified. Methods: Transforming growth factor-β1 (TGF-β1)-activated HSCs LX-2 were single cultured or co-cultured with human umbilical cord mesenchymal stem cells (HUC-MSCs). High-throughput sequencing was used to evaluate the differentially expressed microRNAs (DEMs) between the two groups. Quantitative real-time PCR (qRT-PCR), Western blot, and transfection experiments were used to investigate and screen the most significantly up-regulated DEM. Bioinformatics analysis was used to predict the target mRNAs and the potential functions of the DEM. The possible mechanism of HUC-MSCs against liver fibrosis was analyzed by co-culture experiment of HUC-MSCs with LX-2 cells, and HUC-MSCs treatment of Bile duct ligation (BDL)-induced liver fibrosis in mice. Finally, the mechanism of the DEM regulating liver fibrosis was confirmed in human liver fibrosis specimens. Results: MicroRNA-148a-5p (miR-148a-5p) was the most significantly up-regulated DEM in activated LX-2 cells co-cultured with HUC-MSCs compared with LX-2 cells single cultured. Up-regulation of the expression of miR-148a-5p in activated LX-2 cells could significantly inhibit the expression of hepatic fibrosis markers α-SMA and Col1α1. Notch2 was one target gene of miR-148a-5p. Co-cultured with HUC-MSCs could inhibit the activation of LX-2 cells by inhibiting the expression of the Notch2 and the Notch signaling pathway. In addition, HUC-MSCs treatment could up-regulate the expression of miR-148a-5p in liver tissue and hepatocytes, promote the proliferation and avoid the apoptosis of hepatocytes, and reduce the degree of fibrosis by inhibiting expression of the Notch2 and the Notch signaling pathway in BDL-induced liver fibrosis mice. Moreover, miR-148a-5p was down-regulated and Notch2 was up-regulated in fibrotic human liver tissues compared with the normal livers. Conclusions: HUC-MSCs treatment could inhibit HSCs activation, protect hepatocytes, and alleviate BDL-induced liver fibrosis in mice by up-regulating the expression of miR-148-5p and inhibiting the Notch signaling pathway. The down-regulation of miR-148-5p and up-regulation of Notch2 could be used as biomarkers to monitor the progression of liver fibrosis.
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MSCs promote hepatocyte proliferation and reduce hepatocyte apoptosis via the secretion of hepatotropic factors such as HGF, TGF-β, EGF, NGF, TNF-α, IGF-1, SDF-1, IL-6, IL-10, and PGE2, as well as exosomes, especially microRNAs.
“MSCs promote hepatocyte proliferation and reduce hepatocyte apoptosis via the secretion of hepatotropic factors, such as HGF, TGF-β, EGF, nerve growth factor (NGF), TNF-α, insulin-like growth factor 1 (IGF-1), stromal cell-derived factor 1 (SDF-1), IL-6, IL-10, and prostaglandin E2 (PGE2), as well as exosomes, especially microRNAs (miRs) [96–100].”
From Mechanisms, efficacy, and future perspectives of cellular-based therapies for liver fibrosis/cirrhosis: focusing on mesenchymal stromal cells (2025) · cites this paper as [100]
The Results section on hepatocellular apoptosis and liver regeneration (page unavailable) reports increased Ki-67-positive hepatocytes after HUC-MSC treatment and concludes that treatment inhibits hepatocellular apoptosis in mice with liver fibrosis. The paper also links these effects to increased miR-148a-5p, but the passages do not establish secretion of the listed factors or delivery of microRNAs through exosomes as the mechanism. (LLM, conf=0.89)
Experimental — accuracy not yet measuredIn mouse models, umbilical cord-derived MSCs enhanced proliferation and reduced apoptosis of primary hepatocytes by upregulating miR-148-5p and inhibiting the Notch signaling pathway.
“Zhou et al. reported in mouse models that umbilical cord-derived MSCs (UC-MSCs) enhanced proliferation and reduced apoptosis of primary hepatocytes by upregulating the expression of miR-148-5p and inhibiting the Notch signaling pathway [100].”
From Mechanisms, efficacy, and future perspectives of cellular-based therapies for liver fibrosis/cirrhosis: focusing on mesenchymal stromal cells (2025) · cites this paper as [100]
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- Authors
- Zhou, Q., Rong, C., Gu, T., Li, H., Wu, L., Zhuansun, X., Zhao, X., Xiao, Z., Kuang, Y., Xu, S., & Wang, S.
- Affiliations
- Soochow University (CN)
- Affiliated Hospital of Jiangsu University (CN)
- First Affiliated Hospital of Soochow University (CN)
- Corresponding author
- Xu, Sanrong
- Wang, Shouli
- Venue
- Stem Cell Research & Therapy
- Published
- 2022-07-26
- Volume
- 13
- Issue
- 1
- Pages
- 354-354
- ISSN
- 1757-6512 (ISSN-L)
- PMC
- PMC9327397
- OpenAlex
- W4288074934
- Cited by
- 43
- References
- 45
- Citations by year
- 2026: 5 · 2025: 5 · 2024: 18 · 2023: 14 · 2022: 1
- FWCI
- 5.66
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Stem Cell Research & Therapy (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Key R&D Program of China (2018YFA0107500)
- Zhenjiang Social Development Fund (SH2020027)
- Topics
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Health Sciences › Medicine › Genetics › Mesenchymal stem cell research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Keywords
- mesenchymal stem cells, liver fibrosis, Notch signaling, Notch2, hepatic stellate cells, hepatoprotection, bile duct ligation, hepatocyte proliferation, hepatocyte apoptosis, alpha-smooth muscle actin, type I collagen, human umbilical cord mesenchymal stem cells, co-culture
- MeSH terms
- Animals, Fibrosis, Humans, Liver Cirrhosis, Signal Transduction, Hepatocytes, MicroRNAs, Mice, Hepatic Stellate Cells, Mesenchymal Stem Cells
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