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Cited by 26Extracellular vesicles in diseaseLiver Disease Diagnosis and TreatmentMesenchymal stem cell research

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Huc-MSCs-derived exosomes alleviate non-alcoholic steatohepatitis by regulating macrophages polarization through miR-24-3p/STING axis

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Jiang, Wei, Zeng, Qingmin, Liu, Chang-Hai, Wang, Yonghong, Wang, Shisheng, Chen, Enqiang, Wang, Ming, Zhou, Taoyou, Bai, Lang, Wu, Dongbo, Tang, Hong·2025·Stem Cell Research & Therapy
DOI 10.1186/s13287-025-04197-6PMC PMC11846240
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Abstract

BACKGROUND: There's a scarcity of drugs effective against nonalcoholic steatohepatitis (NASH). Exosomes from Human umbilical cord mesenchymal stem cells (huc-MSCs) show potential in managing glycolipid metabolism and the immune response. Therefore, further investigations are required to explore their application in NASH and the underlying mechanisms. METHODS: C57BL/6J mice were fed with a western diet for 12 weeks to induce NASH, and huc-MSCs exosomes (MSCs-exo) were administered during the feeding period. The effect of MSCs-exo was evaluated by monitoring changes in body weight, fat distribution, blood glucose, and insulin levels, and analyzing pathological alterations in liver tissue. Mechanism investigations were carried out using flow cytometry, immunofluorescence staining, and other experimental techniques. RESULTS: MSCs-exo could reduce liver fat, inflammation, fibrosis, and improved metabolism to alleviate the progression of NASH. Besides, MSCs-exo could decrease macrophage accumulation in the liver, encouraging M2 over M1 macrophage polarization. Furthermore, our study found that MSCs-exo had a high expression of miR-24-3p, which may regulate macrophage polarization by targeting the interferon-stimulated genes (STING) gene in macrophages, with its overexpression amplifying MSCs-exo's NASH benefits. CONCLUSIONS: These findings suggest that the therapeutic effect of MSCs-exo on NASH may be attributed to the regulation of macrophage M2 polarization through miR-24-3p targeting STING. This provides a scientific basis for future clinical application.

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Fig. 1 MSCs-derived exosome (MSCs-Exo) relieve lipid deposition in NASH mice. A. Identification of multidirectional differentiation of MSCs. Adipogenesis differentiation ability was detected by oil red staining; Osteogenesis differentiation ability was detected by alizarin red staining; Hepatocyte-like differentiation ability was detected by glycogen staining; CD90 expression levels were examined by flow cytometry. B. Representative transmission electron microscopic images of hUC-MSCs-Exo; C. Western blot analysis of the surface hUC-MSCs-Exo markers CD9 and CD81. Full-length blots are presented in supplementary figure S3. D. Experimental workflow diagram for the treatment of NASH mice with MSCs-Exo. E and F. Glucose (mmol/L) and insulin (ng/ml) levels of mice in NC, WD and WDE. G. Hematoxylin & eosin (H&E) staining, Oil Red staining, Masson’s trichrome staining, and micro-CT imaging of liver tissues from NC, WD and WDE mice. The differences between groups were calculated using ANOVA (n = 5). *p < 0.05, **p < 0.01, ***p < 0.001. Abbreviations: NASH, nonalcoholic steatohepatitis; MSCs, mesenchymal stem cells; Exo, exosome; NC, control group; WD, western diet group; WDE, exosome treatment group
Fig. 1 MSCs-derived exosome (MSCs-Exo) relieve lipid deposition in NASH mice. A. Identification of multidirectional differentiation of MSCs. Adipogenesis differentiation ability was detected by oil red staining; Osteogenesis differentiation ability was detected by alizarin red staining; Hepatocyte-like differentiation ability was detected by glycogen staining; CD90 expression levels were examined by flow cytometry. B. Representative transmission electron microscopic images of hUC-MSCs-Exo; C. Western blot analysis of the surface hUC-MSCs-Exo markers CD9 and CD81. Full-length blots are presented in supplementary figure S3. D. Experimental workflow diagram for the treatment of NASH mice with MSCs-Exo. E and F. Glucose (mmol/L) and insulin (ng/ml) levels of mice in NC, WD and WDE. G. Hematoxylin & eosin (H&E) staining, Oil Red staining, Masson’s trichrome staining, and micro-CT imaging of liver tissues from NC, WD and WDE mice. The differences between groups were calculated using ANOVA (n = 5). *p < 0.05, **p < 0.01, ***p < 0.001. Abbreviations: NASH, nonalcoholic steatohepatitis; MSCs, mesenchymal stem cells; Exo, exosome; NC, control group; WD, western diet group; WDE, exosome treatment groupCC BY-NC-ND · PubMed Central
Fig. 2 Macrophages are involved in the pathogenesis of NASH. A. Immunofluorescence (IF) staining of CD68 in normal human liver samples and NASH patients’ liver samples. B. IF staining of F4/80 in the liver tissue of NC and WD mice. C. Flow cytometry analysis of F4/80+ and CD11b+ macrophages in the liver tissue of NC, WD mice. D. Quantitative analysis of F4/80+/CD11b+ in the liver tissue of NC, WD mice. E. Experimental workflow diagram for the treatment of NASH mice with MSCs-Exo, with or without macrophage scavenger (clodronate liposome). The clodronate liposome treatment group was named WDM. F, G. Glucose (mmol/L) and insulin (ng/ml) levels of mice in NC, WD and WDM. H. H&E staining, Oil Red staining, Masson’s trichrome staining, and micro-CT imaging of liver tissues from NC, WD and WDM mice. The differences between groups were calculated using ANOVA (n = 5). *p < 0.05. Abbreviations: NASH, nonalcoholic steatohepatitis; NC, control group; WD, western diet group; WDE, exosome treatment group
Fig. 2 Macrophages are involved in the pathogenesis of NASH. A. Immunofluorescence (IF) staining of CD68 in normal human liver samples and NASH patients’ liver samples. B. IF staining of F4/80 in the liver tissue of NC and WD mice. C. Flow cytometry analysis of F4/80+ and CD11b+ macrophages in the liver tissue of NC, WD mice. D. Quantitative analysis of F4/80+/CD11b+ in the liver tissue of NC, WD mice. E. Experimental workflow diagram for the treatment of NASH mice with MSCs-Exo, with or without macrophage scavenger (clodronate liposome). The clodronate liposome treatment group was named WDM. F, G. Glucose (mmol/L) and insulin (ng/ml) levels of mice in NC, WD and WDM. H. H&E staining, Oil Red staining, Masson’s trichrome staining, and micro-CT imaging of liver tissues from NC, WD and WDM mice. The differences between groups were calculated using ANOVA (n = 5). *p < 0.05. Abbreviations: NASH, nonalcoholic steatohepatitis; NC, control group; WD, western diet group; WDE, exosome treatment groupCC BY-NC-ND · PubMed Central
Fig. 3 MSCs-exo alleviate NASH by regulating macrophage function. A. IF staining of F4/80 in the liver tissue of NC, WD, and WDE mice. B. Flow cytometry analysis of F4/80+ and CD11b+ macrophages in the liver tissue of NC, WD, and WDE mice. C. Flow cytometry analysis of CD206− and CD11c+ macrophages in the liver tissue of NC, WD, and WDE mice. D and E. Quantitative analysis of CD206−/ CD11c+ and CD11c−/CD206+ in the liver tissue of NC, WD, and WDE mice. F. qRT-PCR analysis of the expression of TNF-α, IL-1β, Arg1, and CD206 in the liver tissue of NC, WD, and WDE mice. The differences between groups were calculated using ANOVA (n = 5). *p < 0.05, **p < 0.01, ***p < 0.001. Abbreviations: NASH, nonalcoholic steatohepatitis; MSCs, mesenchymal stem cells; Exo, exosome; NC, control group; WD, western diet group; WDE, exosome treatment group
Fig. 3 MSCs-exo alleviate NASH by regulating macrophage function. A. IF staining of F4/80 in the liver tissue of NC, WD, and WDE mice. B. Flow cytometry analysis of F4/80+ and CD11b+ macrophages in the liver tissue of NC, WD, and WDE mice. C. Flow cytometry analysis of CD206− and CD11c+ macrophages in the liver tissue of NC, WD, and WDE mice. D and E. Quantitative analysis of CD206−/ CD11c+ and CD11c−/CD206+ in the liver tissue of NC, WD, and WDE mice. F. qRT-PCR analysis of the expression of TNF-α, IL-1β, Arg1, and CD206 in the liver tissue of NC, WD, and WDE mice. The differences between groups were calculated using ANOVA (n = 5). *p < 0.05, **p < 0.01, ***p < 0.001. Abbreviations: NASH, nonalcoholic steatohepatitis; MSCs, mesenchymal stem cells; Exo, exosome; NC, control group; WD, western diet group; WDE, exosome treatment groupCC BY-NC-ND · PubMed Central
Fig. 4 MSCs-exo regulate macrophage polarity through the STING signaling pathway. A. Immunofluorescence co-localization of STING and CD68 in normal human liver samples and NASH patients. B. Immunofluorescence co-localization of STING and F4/80 of liver tissue from NC and WD mice. C. H&E staining, Oil Red staining, Masson’s trichrome staining, and micro-CT imaging of liver tissues from WD, WDD and WDED mice. D. Flow cytometry analysis of CD206− and CD11c+ macrophages in the liver tissue of WD, WDD and WDED mice. E and F. Quantitative analysis of CD206−/ CD11c+ and CD11c−/CD206+ in the liver tissue of WD, WDD and WDED mice. G. Western blot analysis of STING in the liver tissue of WD, WDD and WDED mice. Full-length blots are presented in supplementary figure S4. The differences between groups were calculated using ANOVA (n = 5). *p < 0.05. Abbreviations: MSCs, mesenchymal stem cells; Exo, exosome; NC, control group; WD, western diet group; WDE, exosome treatment group. WDD, STING agonist (DMXAA) treatment group; WDED, DMXAA and exosomes treatment group.
Fig. 4 MSCs-exo regulate macrophage polarity through the STING signaling pathway. A. Immunofluorescence co-localization of STING and CD68 in normal human liver samples and NASH patients. B. Immunofluorescence co-localization of STING and F4/80 of liver tissue from NC and WD mice. C. H&E staining, Oil Red staining, Masson’s trichrome staining, and micro-CT imaging of liver tissues from WD, WDD and WDED mice. D. Flow cytometry analysis of CD206− and CD11c+ macrophages in the liver tissue of WD, WDD and WDED mice. E and F. Quantitative analysis of CD206−/ CD11c+ and CD11c−/CD206+ in the liver tissue of WD, WDD and WDED mice. G. Western blot analysis of STING in the liver tissue of WD, WDD and WDED mice. Full-length blots are presented in supplementary figure S4. The differences between groups were calculated using ANOVA (n = 5). *p < 0.05. Abbreviations: MSCs, mesenchymal stem cells; Exo, exosome; NC, control group; WD, western diet group; WDE, exosome treatment group. WDD, STING agonist (DMXAA) treatment group; WDED, DMXAA and exosomes treatment group.CC BY-NC-ND · PubMed Central
Fig. 5 MSCs-exo carrying miR-24-3p regulate STING signaling pathway to alleviate NASH. A. qRT-PCR analysis of the expression of 9 miRNA candidates in the lysates from MSCs-Exo. B. Schematic diagram of the binding sites between miR-24-3p and wild-type STING 3’UTR (h-sting-3UTR-wt) or mutant (h-sting-3UTR-mu), and conservation analysis of the seed sequence. C. Luciferase reporter assays were used to confirm the combination between miR-24-3p and STING 3’UTR. D. H&E staining, Oil Red staining, Masson’s trichrome staining, and micro-CT imaging of liver tissues from WD, WDE and WDE-miR-24 mice. E. Flow cytometry analysis of CD206−, CD11c+ macrophages in the liver tissue of WD, WDE and WDE-miR-24 mice. F, G. Quantitative analysis of CD206−/ CD11c+ and CD11c−/CD206+ in the liver tissue of WD, WDE and WDE-miR-24 mice. H. Flow cytometry analysis of Arg1+ macrophages in the RAW of Ctrl, EVs, EVs + Agomir and EVs + Antagomir. I. Quantitative analysis of Arg1+ macrophages in the RAW of Ctrl, EVs, EVs + Agomir and EVs + Antagomir. The differences between groups were calculated using ANOVA (n = 5). *p < 0.05, **p < 0.01. Abbreviations: MSCs, mesenchymal stem cells; Exo, exosome; NC, control group; WD, western diet group; WDE, exosome treatment group. WDE, exosome treatment group; WDE-miR-24, miR-24-3p-rich exosomes treatment group
Fig. 5 MSCs-exo carrying miR-24-3p regulate STING signaling pathway to alleviate NASH. A. qRT-PCR analysis of the expression of 9 miRNA candidates in the lysates from MSCs-Exo. B. Schematic diagram of the binding sites between miR-24-3p and wild-type STING 3’UTR (h-sting-3UTR-wt) or mutant (h-sting-3UTR-mu), and conservation analysis of the seed sequence. C. Luciferase reporter assays were used to confirm the combination between miR-24-3p and STING 3’UTR. D. H&E staining, Oil Red staining, Masson’s trichrome staining, and micro-CT imaging of liver tissues from WD, WDE and WDE-miR-24 mice. E. Flow cytometry analysis of CD206−, CD11c+ macrophages in the liver tissue of WD, WDE and WDE-miR-24 mice. F, G. Quantitative analysis of CD206−/ CD11c+ and CD11c−/CD206+ in the liver tissue of WD, WDE and WDE-miR-24 mice. H. Flow cytometry analysis of Arg1+ macrophages in the RAW of Ctrl, EVs, EVs + Agomir and EVs + Antagomir. I. Quantitative analysis of Arg1+ macrophages in the RAW of Ctrl, EVs, EVs + Agomir and EVs + Antagomir. The differences between groups were calculated using ANOVA (n = 5). *p < 0.05, **p < 0.01. Abbreviations: MSCs, mesenchymal stem cells; Exo, exosome; NC, control group; WD, western diet group; WDE, exosome treatment group. WDE, exosome treatment group; WDE-miR-24, miR-24-3p-rich exosomes treatment groupCC BY-NC-ND · PubMed Central
Fig. 6 The potential mechanism of mesenchymal stem cell-derived exosomes (MSCs-exo) in treating nonalcoholic steatohepatitis (NASH). Western diet can induce M1 polarization of macrophages in liver, release inflammatory factors, and promote the formation and progression of NASH. MSCs-exo can induce M2 polarization of macrophages, reduce the release of inflammatory factors, and alleviate the formation and progression of NASH. The mechanism may be that exosomes-derived miR-24-3p regulates STING signaling pathway in macrophages
Fig. 6 The potential mechanism of mesenchymal stem cell-derived exosomes (MSCs-exo) in treating nonalcoholic steatohepatitis (NASH). Western diet can induce M1 polarization of macrophages in liver, release inflammatory factors, and promote the formation and progression of NASH. MSCs-exo can induce M2 polarization of macrophages, reduce the release of inflammatory factors, and alleviate the formation and progression of NASH. The mechanism may be that exosomes-derived miR-24-3p regulates STING signaling pathway in macrophagesCC BY-NC-ND · PubMed Central

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Metadata

Authors
Jiang, W., Zeng, Q., Liu, C.-H., Wang, Y., Wang, S., Chen, E., Wang, M., Zhou, T., Bai, L., Wu, D., & Tang, H.
Affiliations
Sichuan University (CN)
Corresponding author
  • Wu, Dongbo
  • Tang, Hong
ORCID
Venue
Stem Cell Research & Therapy
Publisher
Springer Science and Business Media LLC
Published
2025-02-21
Volume
16
Issue
1
Pages
74-74
ISSN
1757-6512 (ISSN-L)
DOI
10.1186/s13287-025-04197-6
PMC
PMC11846240
OpenAlex
W4407842915
Cited by
26
References
2
Citations by year
2026: 15 · 2025: 11
FWCI
7.82
Type
journal article
Language
en
Open access
Licence
Locations
  • Stem Cell Research & Therapy (publishedVersion, cc-by-nc-nd)
  • PubMed Central (publishedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
Funders
  • National Key Research and Development Program of China (2022YFC2304800)
  • 1.35 project for disciplines of excellence, West China Hospital, Sichuan University (ZYGD23030)
  • National Natural Science Foundation of China (82172254, 81900512)
  • the Science and Technological Supports Project of Sichuan Province, China (2024NSFSC1690)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Extracellular vesicles in disease
  • Health Sciences › Medicine › Hepatology › Liver Disease Diagnosis and Treatment
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Mesenchymal stem cell research
Keywords
nonalcoholic steatohepatitis, exosomes, human umbilical cord mesenchymal stem cells, macrophage polarization, M2 macrophages, miR-24-3p, STING, liver fibrosis, liver inflammation, lipid metabolism
MeSH terms
STING Protein, Animals, Humans, Liver, Macrophages, Male, Membrane Proteins, Mice, Inbred C57BL, Umbilical Cord, MicroRNAs, Mice, Exosomes, Mesenchymal Stem Cells, Non-alcoholic Fatty Liver Disease

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