ArticleMolecular biology reports2021
RNA sequencing of LX-2 cells treated with TGF-β1 identifies genes associated with hepatic stellate cell activation.
Article in Molecular biology reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
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- Procollagen 1 assembles into phase-separated condensates in the endoplasmic reticulum.The Journal of cell biology · 2026Article
- A thioacrylamide-based compound directly counteracts hepatic fibrosis with profound anti-obesity action.JHEP reports : innovation in hepatology · 2026Article
- Hepatic-stellate-cell-targeted delivery of PU.1 decoy ODN by Apt-Tan attenuates liver fibrosis in mice.Molecular therapy. Nucleic acids · 2025Article
- Amniotic Fluid Reduces Liver Fibrosis By Attenuating Hepatic Stellate Cell Activation.bioRxiv : the preprint server for biology · 2025Article
- Amniotic fluid reduces liver fibrosis by attenuating hepatic stellate cell activation.Stem cells translational medicine · 2025Article
- Article
- Identification of biomarkers for the diagnosis of type 2 diabetes mellitus with metabolic associated fatty liver disease by bioinformatics analysis and experimental validation.Frontiers in endocrinology · 2025Article
- The acidic microenvironment in the perisinusoidal space critically determines bile salt-induced activation of hepatic stellate cells.Communications biology · 2024Article
- Formation and Investigation of Cell-Derived Nanovesicles as Potential Therapeutics against Chronic Liver Disease.Advanced healthcare materials · 2023Article
- The NaCellular and molecular life sciences : CMLS · 2021Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundHepatic stellate cells (HSCs) are liver-resident myofibroblast precursors responsible for the production of collagen and maintenance of the hepatic extracellular matrix (ECM). As such, they are generally associated with fibrotic liver diseases. HSCs become "activated" in response to tissue damage or pathogen invasion, a process most commonly driven by transforming growth factor-β1 (TGF-β1). Despite this, the full extent of TGF-β1 signalling in these cells is poorly understood. Clarifying the range and diversity of this signalling will further improve our understanding of the process of HSC activation. METHODS AND
resultsRNA sequencing was used to quantitate the transcriptomic changes induced in LX-2 cells, an activated human HSC line, following TGF-b1 treatment. In total, 5,258 genes were found to be significantly differentially expressed with a false discovery rate cut-off of < 0.1. The topmost deregulated of these genes included those with no currently characterised role in either HSC activation or fibrotic processes, including CIITA and SERPINB2. In silico analysis revealed the prominent signalling pathways downstream of TGF-β1 in LX-2 cells.
conclusionsIn this study, we describe the genes and signalling pathways significantly deregulated in LX-2 cells following TGF-β1 treatment. We identified several highly deregulated genes with no currently characterised role in HSC activation, which may represent novel mediators of fibrotic responses in HSCs or the liver macroenvironment. This work may be of use in the identification of new markers of liver fibrosis and could provide insight into prospective genes or pathways that might be targeted for the amelioration of fibrotic liver disease in the future.
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