Antidiabetic thiazolidinediones inhibit collagen synthesis and hepatic stellate cell activation in vivo and in vitro
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Background & aims The ligand-dependent transcription factor peroxisome proliferator-activated receptor gamma (PPARgamma) is expressed in hepatic stellate cells (HSC), and its transcriptional activity is reduced during cell transdifferentiation in culture. PPARgamma transcriptional activation decreases platelet-derived growth factor-induced proliferation and inhibits alpha-smooth muscle actin expression in cultured HSC. The aim of our study was to evaluate whether oral administration of synthetic PPARgamma ligands, thiazolidinediones (TZD), might affect collagen deposition in animal models of liver fibrosis.Methods The effect of 2 TZD (pioglitazone or rosiglitazone) was tested on liver fibrosis induced in rats by either toxin administration (dimethylnitrosamine or carbon tetrachloride) or bile duct ligation. In vivo PPARgamma activation was evaluated by gel shift assay using nuclear extracts from HSC isolated from control and treated rats.Results Oral administration of TZD reduced extracellular matrix deposition and HSC activation in both toxic and cholestatic models of liver fibrosis. PPARgamma-specific DNA binding was significantly impaired in nuclear extracts of HSC isolated from fibrotic rats compared with HSC from control rats. TZD administration restored PPARgamma DNA binding in HSC nuclei. In vitro, TZD-induced PPARgamma activation inhibited collagen and fibronectin synthesis induced by transforming growth factor (TGF)-beta1 in human HSC, as measured by enzyme-linked immunosorbent assay and Northen blotting. TZD also reduced the TGF-beta1-induced activity of a 3.5-kilobase procollagen type I promoter transfected in human HSC.Conclusions These findings indicate that PPARgamma activation in HSC retards fibrosis in vivo and suggest the use of TZD for the treatment of liver fibrosis.
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In different mouse models of induced liver fibrosis (carbon tetrachloride/dimethylnitrosamine intoxication and bile duct ligation), the synthetic PPAR-γ ligand thiazolidinedione was linked to a reduction of extracellular matrix deposition and hepatic stellate cell activation.
“The change of HSC phenotype was further investigated in different mouse models of induced liver fibrosis (CCl 4 /dimethylnitrosamine intoxication and bile duct ligation) in which the synthetic PPAR-γ ligand thiazolidinedione was linked to a reduction of ECM deposition and HSC activation.[130]”
From Nuclear receptors in liver fibrosis (2021) · cites this paper as [130]
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- Authors
- Galli, A., Crabb, D. W., Ceni, E., Salzano, R., Mello, T., Svegliati–Baroni, G., Ridolfi, F., Trozzi, L., Surrenti, C., & Casini, A.
- Affiliations
- University of Florence (IT)
- Indiana University Indianapolis (US)
- Venue
- Gastroenterology
- Publisher
- Elsevier BV
- Published
- 2002-06
- Volume
- 122
- Issue
- 7
- Pages
- 1924-1940
- ISSN
- 0016-5085 (ISSN-L)
- OpenAlex
- W2031054297
- Cited by
- 440
- References
- 78
- Citations by year
- 2026: 3 · 2025: 5 · 2024: 8 · 2023: 14 · 2022: 7 · 2021: 18 · 2020: 13 · 2019: 7 · 2018: 12 · 2017: 15 · 2016: 15 · 2015: 13 · 2014: 20 · 2013: 22 · 2012: 19
- FWCI
- 19.30
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Gastroenterology (publishedVersion)
- PubMed (publishedVersion)
- Florence Research (University of Florence) (submittedVersion)
- Università Politecnica delle Marche (Università Politecnica delle Marche) (submittedVersion)
- Topics
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
- Keywords
- thiazolidinediones, PPARγ, hepatic stellate cells, liver fibrosis, collagen synthesis, fibronectin, pioglitazone, rosiglitazone, TGF-β1, extracellular matrix deposition, carbon tetrachloride, N-nitrosodimethylamine, bile duct ligation, antifibrotic therapy
- MeSH terms
- Rosiglitazone, Pioglitazone, Bisphenol A Compounds, Animals, Benzhydryl Compounds, Bile Ducts, Carbon Tetrachloride, Cell Division, Cells, Cultured, Collagen, Dimethylnitrosamine, DNA, Epoxy Compounds, Fibronectins, Hypoglycemic Agents, Ligation, Liver, Liver Cirrhosis, Male, Phenols, Promoter Regions, Genetic, Thiazoles, Transcription Factors, Rats, Sprague-Dawley, Receptors, Cytoplasmic and Nuclear, Thiazolidinediones, Rats
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