ArticleExperimental and therapeutic medicine2019
MicroRNA-122 inhibits epithelial-mesenchymal transition of hepatic stellate cells induced by the TGF-β1/Smad signaling pathway.
Article in Experimental and therapeutic medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 17 citations in OpenAlex.
- Evaluation of miRNA Expression in Pediatric Cirrhosis Caused by BA and PFIC.BioMed research international · 2026Article
- Engineered mesenchymal stem cell-derived exosomes: A revolutionary approach to unlocking liver disease treatment.Biochemistry and biophysics reports · 2025Review
- Co-allosteric hairpin probe for detecting microRNA with high specificity.RSC advances · 2025Article
- Regulatory Roles and Therapeutic Potential of miR-122-5p in Hypoxic-Ischemic Brain Injury: Comprehensive Review.Cell biochemistry and biophysics · 2025Review
- Article
- The Role of TGF-β/SMAD Signaling in Hepatocellular Carcinoma: from Mechanism to Therapy and Prognosis.International journal of biological sciences · 2024Review
- Interplays of liver fibrosis-associated microRNAs: Molecular mechanisms and implications in diagnosis and therapy.Genes & diseases · 2023Review
- Review
- Molecular Targets and Signaling Pathways of microRNA-122 in Hepatocellular Carcinoma.Pharmaceutics · 2022Review
- Exosomal microRNA-618 derived from mesenchymal stem cells attenuate the progression of hepatic fibrosis by targeting Smad4.Bioengineered · 2022Article
- [Regulatory effects of microRNAs on hepatic stellate cell activation and liver fibrogenesis].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2021Article
- MicroRNAs as crucial mediators in the pharmacological activities of triptolide (Review).Experimental and therapeutic medicine · 2021Review
- Up-regulation of FUT8 inhibits TGF-β1-induced activation of hepatic stellate cells during liver fibrogenesis.Glycoconjugate journal · 2021Article
- The Epithelial-to-Mesenchymal Transition as a Possible Therapeutic Target in Fibrotic Disorders.Frontiers in cell and developmental biology · 2020Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transforming growth factor (TGF)-β1 may stimulate the activation of hepatic stellate cells (HSCs), resulting in the development of liver fibrosis. As micro RNA (miRNA)-122 is known to be associated with liver inflammation, its effects on the epithelial-mesenchymal transition (EMT) of HSCs through the inhibition of the TGF-β1/drosophila mothers against decapentaplegic protein 4 (Smad4) signaling pathway were investigated. The MTT assay was performed to explore the optimum TGF-β1 concentration suitable for HSC stimulation. Fluorescence microscopy was used to observe the transfection efficiency and reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blot analysis were used to observe gene and protein expression levels of α-smooth muscle actin (α-SMA), E-cadherin, N-cadherin and Smad4, respectively, in HSCs treated with TGF-β1 or TGF-β1 and miRNA-122. MTT assay results indicated that the concentration of 10 µg/l TGF-β1 was suitable for maximum growth and survival of HSCs. Notably, the mRNA expression levels of N-cadherin and α-SMA were significantly increased (each, P<0.05), but the expression levels of E-cadherin were decreased following 10 µg/l TGF-β1 treatment. Similar results were observed regarding the protein expression levels of N-cadherin, α-SMA and E-cadherin. Furthermore, the expression of F-actin was increased in the 10 µg/l TGF-β1 treated group compared with the 0 µg/l TGF-β1 treaded group and stretching of the muscle fiber filament was observed. miRNA-122 lentiviral vector transfection significantly decreased the mRNA expression of N-cadherin and increased the mRNA expression of E-cadherin in HSCs stimulated with TGF-β1, as evident from RT-qPCR results. Similar results were also observed regarding the protein expression levels of N-cadherin and E-cadherin. The expression levels of Smad4, the primary component of the TGF-β1 signaling pathway, were significantly lower in cells treated with TGF-β1 and miRNA-122 (P<0.01) compared those treated with TGF-β1. Thus, miRNA-122 may inhibit the activation and EMT of HSCs stimulated by TGF-β1.
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