Project description:We found that the number of tumor-infiltrating myofibroblasts was positively correlated to tumor acidification status in hepatocellular carcinoma (HCC). Hepatic stellate cells (HSCs), the predominant precursors of liver myofibroblasts, were activated and transdifferentiated into myofibroblasts under acidic culture condition. To identify the molecular phenotype of LX-2 cells in acidic culture conditions, we further conducted a gene expression profile analysis.
Project description:We found that the number of tumor-infiltrating myofibroblasts was positively correlated to tumor acidification status in hepatocellular carcinoma (HCC). Hepatic stellate cells (HSCs), the predominant precursors of liver myofibroblasts, were activated and transdifferentiated into myofibroblasts under acidic culture condition. To identify the molecular phenotype of LX-2 cells in acidic culture conditions, we further conducted a gene expression profile analysis. LX-2 cells cultured in pH 7.2 or pH 6.2 medium separately for six days was used in gene expression microarray analysis.
Project description:Hepatic stellate cell activation is a major driver of extracellular matrix deposition during liver fibrosis. This study investigated the transcriptional changes induced by ATP6AP1 depletion in human hepatic stellate LX-2 cells. LX-2 cells were transfected with ATP6AP1-targeting siRNA or non-targeting control siRNA, with three independent biological replicates per condition. Total RNA was extracted and subjected to RNA sequencing. Sequencing reads were aligned to the human reference genome GRCh38.p10, and differential gene-expression analysis was performed using DESeq2. The dataset was generated to identify the cellular pathways regulated by ATP6AP1 depletion, with particular emphasis on hepatic stellate cell activation, cellular senescence, cell-cycle arrest and Notch signaling
Project description:To investigate the role of AEBP1 involved in hepatic stellate cells (HSCs), we inhibited AEBP1 expression by specific siRNA in human HSC line LX-2 cells. Total RNA was loaded for bulk RNA sequencing.
Project description:Hepatic fibrosis is the strongest contributor to hepatocarcinogenesis in metabolic dysfunction-associated steatotic liver disease (MASLD); however, the underlying mechanisms have yet to be fully elucidated. In 94 human MASLD biopsy samples, artificial intelligence-based morphological phenotyping of hepatic fiber and multi-omics analyses revealed that insulin growth factor-binding protein 7 (IGFBP-7) secreted from senescent periportal endothelial cells might transform stellate cells into a hepatocarcinogenesis-promoting phenotype. To test the effect of IGFBP-7 on HSC, a hepatic stellate cell line, LX-2, was cultured with recombinant IGFBP-7 (100ng/mL), resulting in their transformation to a more activated form than the control.
Project description:Expression data from the hepatic stellate cell line LX-2 after treatment with the prolylhydroxylase inhibitor dimethyloxalylglycine (DMOG) and from the liver sinusoidal endothelial cell line TRP3 after incubation with conditioned medium of DMOG-treated LX-2 Prolyl-hydroxylase inhibitors such as dimethyloxalylglycine (DMOG) stabilize HIF-1α, thereby chemically inducing hypoxia, which also accelerates liver volume increase when given with portal rerouting. We used microarrays to clarify the cellular crosstalk of the different cell types in accelerated liver regeneration by examining the role of hepatic stellate cells (HSC) and liver sinusoidal endothelial cells (LSEC).
Project description:Hepatic stellate cell (HSC) activation is a key driver of liver fibrogenesis, but the transcriptional response to bone morphogenetic protein 5 (BMP5) in these cells has not been systematically characterized. To address this, we performed RNA‑sequencing on the human LX‑2 hepatic stellate cell line following stimulation with recombinant BMP5 protein, compared with vehicle‑treated controls. Each condition included five independent biological replicates to ensure statistical robustness. Total RNA was extracted, and strand‑specific libraries were prepared for high‑throughput sequencing. This dataset enables the genome‑wide identification of differentially expressed genes, pathway enrichment analyses, and the delineation of BMP5‑regulated networks in HSCs. Our transcriptomic profiles provide a comprehensive resource for understanding the molecular actions of BMP5 in hepatic fibrosis and may reveal potential targets for therapeutic intervention.
Project description:Hepatic stellate cells(HSCs) are the main effector cells of liver fibrosis. In order to study the effect of mesenchymal stem cells(MSCs) on microRNAs expression of HSCs, we co-cultured HSCs LX-2 activated by TGFβ1 with human umbilical cord MSCs(hUC-MSCs) for 48 hours, and compared the differentially expressed miRNA with LX-2 cultured alone by high-throughput sequencing. The results showed that two mature microRNAs expressed increased, and nine expressed decreased.
