ArticleJournal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban2010
All-trans retinoic acid diminishes collagen production in a hepatic stellate cell line via suppression of active protein-1 and c-Jun N-terminal kinase signal.
Article in Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 27 citations in OpenAlex.
- Rhein from a traditional herbal formula attenuates hepatic fibrosis via ALDH1A3-mediated retinoic acid metabolism.Chinese medicine · 2026Article
- Resolving fibrosis by stimulating HSC-dependent extracellular matrix degradation.Science translational medicine · 2025Article
- LX-2 Stellate Cells Are a Model System for Investigating the Regulation of Hepatic Vitamin A Metabolism and Respond to Tumor Necrosis FactorDrug metabolism and disposition: the biological fate of chemicals · 2024Article
- Retinoic Acid Signaling in Fatty Liver Disease.Liver research (Beijing, China) · 2023Article
- Article
- Altered vitamin A metabolism in human liver slices corresponds to fibrogenesis.Clinical and translational science · 2021Article
- Hepatic Stellate Cell Activation and Inactivation in NASH-Fibrosis-Roles as Putative Treatment Targets?Biomedicines · 2021Review
- Retinoic Acid: A New Old Friend of IL-17A in the Immune Pathogeny of Liver Fibrosis.Frontiers in immunology · 2021Review
- Modulation of retinoid signaling: therapeutic opportunities in organ fibrosis and repair.Pharmacology & therapeutics · 2020Review
- Dynamic changes of activator protein 1 and collagen I expression in the sclera of myopia guinea pigs.International journal of ophthalmology · 2019Article
- In vitro inhibition of hepatic stellate cell activation by the autophagy-related lipid droplet protein ATG2A.Scientific reports · 2018Article
- Senescence in hepatic stellate cells as a mechanism of liver fibrosis reversal: a putative synergy between retinoic acid and PPAR-gamma signalings.Clinical and experimental medicine · 2017Review
- The association between nuclear receptors and ocular diseases.Oncotarget · 2017Review
- Potential role of nuclear receptor ligand all-trans retinoic acids in the treatment of fungal keratitis.International journal of ophthalmology · 2015Review
- Review
- The controversial role of retinoic acid in fibrotic diseases: analysis of involved signaling pathways.International journal of molecular sciences · 2012Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Following acute and chronic liver injury, hepatic stellate cells (HSCs) become activated to undergo a phenotypic transformation into myofibroblast-like cells and lose their retinol content, but the mechanisms of retinoid loss and its potential roles in HSCs activation and liver fibrosis are not understood. The influence of retinoids on HSCs and hepatic fibrosis remains controversial. The purpose of this study was to evaluate the effects of all-trans retinoid acid (ATRA) on cell proliferation, mRNA expression of collagen genes [procollagen α1 (I), procollagen α1 (III)], profibrogenic genes (TGF-β(1), CTGF, MMP-2, TIMP-1, TIMP-2, PAI-1), fibrolytic genes (MMP-3, MMP-13) and the upstream element (JNK and AP-1) in the rat hepatic stellate cell line (CFSC-2G). Cell proliferation was evaluated by measuring BrdU incorporation. The mRNA expression levels of collagen genes [procollagen α1 (I), procollagen α1 (III)], profibrogenic genes (TGF-β(1), CTGF, MMP-2, TIMP-1, TIMP-2, PAI-1), and fibrolytic genes (MMP-3, MMP-13) were quantitatively detected by using real-time PCR. The mRNA expression of JNK and AP-1 was quantified by RT-PCR. The results showed that ATRA inhibited HSCs proliferation and diminished the mRNA expression of collagen genes [procollagen α1 (I), procollagen α1 (III)] and profibrogenic genes (TGF-β(1), CTGF, MMP-2, TIMP-1, TIMP-2, PAI-1), and significantly stimulated the mRNA expression of MMP-3 and MMP-13 in HSCs by suppressing the mRNA expression of JNK and AP-1. These findings suggested that ATRA could inhibit proliferation and collagen production of HSCs via the suppression of active protein-1 and c-Jun N-terminal kinase signal, then decrease the mRNAs expression of profibrogenic genes (TGF-β(1), CTGF, MMP-2, TIMP-1, TIMP-2, PAI-1), and significantly induce the mRNA expression of MMP-3 and MMP-13.
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