98%
921
2 minutes
20
The immortal murine hepatic stellate cell line Col-GFP HSC was comprehensively characterized using genetic and molecular approaches. Short tandem repeat (STR) profiling and karyotyping combined with multiplex fluorescence in situ hybridization (M-FISH) confirmed the identity of the cell line and revealed no contamination. Col-GFP HSCs showed a near tetraploid karyotype. Additionally, next-generation sequencing (NGS) data, quantitative reverse transcription PCR, and Western blot analyses demonstrated robust expression of genes and proteins associated with hepatic stellate cells, including those involved in extracellular matrix remodeling and fibrogenic pathways. Phalloidin staining revealed filamentous actin patterns characteristic of stellate cells, providing additional support for their cytoskeletal organization and functional status. These findings provide strong evidence that the Col-GFP HSC cell line originates from hepatic stellate cells and can serve as a reliable in vitro model to study stellate cell biology and related pathophysiological processes.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC12386721 | PMC |
http://dx.doi.org/10.3390/ijms26167764 | DOI Listing |
Sci Transl Med
September 2025
Department of Medicine, Columbia University Irving Medical Center, New York, NY 10032, USA.
Hepatocyte apoptosis is a key feature of metabolic dysfunction-associated steatohepatitis (MASH), but the fate of apoptotic hepatocytes in MASH is poorly understood. Here, we explore the hypotheses that clearance of dead hepatocytes by liver macrophages (efferocytosis) is impaired in MASH because of low expression of the efferocytosis receptor T cell immunoglobulin and mucin domain containing 4 (TIM4; gene ) by MASH liver macrophages, which then drives liver fibrosis in MASH. We show that apoptotic hepatocytes accumulate in human and experimental MASH, using mice fed the fructose-palmitate-cholesterol (FPC) diet or the high-fat, choline-deficient amino acid-defined (HF-CDAA) diet.
View Article and Find Full Text PDFLiver Int
October 2025
TGF-Beta and Cancer Group - Oncobell Program, Bellvitge Biomedical Research Institute (IDIBELL), L'Hospitalet de Llobregat, Barcelona, Spain.
Background And Aims: Hepatocellular carcinoma (HCC) has a poor prognosis and limited treatment options. TGF-β is a promising therapeutic target, but its dual role, as both a tumour suppressor and promoter, complicates its clinical application. While its effects on tumour cells are increasingly understood, its impact on the tumour stroma remains unclear.
View Article and Find Full Text PDFCell Mol Immunol
September 2025
Department of Gastroenterology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, 200120, China.
Gut-derived metabolites are essential for liver fibrogenesis. The aim of this study was to determine the alteration of indole-3-propionic acid (IPA), a crucial tryptophan metabolite, in liver fibrosis and delineate the roles of enterogenic IPA in fibrogenesis. In the present study, metabolomics assays focused on tryptophan metabolism were applied to explore the decreased levels of IPA in the feces and serum of cirrhotic patients, as well as in the feces and portal vein serum of fibrotic mice.
View Article and Find Full Text PDFJ Gastroenterol
September 2025
Department of General Surgery (Hepatopancreatobiliary Surgery), Department of Biliary-Pancreatic Center, The Affiliated Hospital of Southwest Medical University, 25 Taiping Street, Jiangyang District, Luzhou City, 646000, Sichuan Province, China.
Background And Aims: Inflammatory cell infiltration in the liver is a hallmark of metabolic dysfunction-associated fatty liver disease (MAFLD). However, the pathological events that trigger the infiltration of inflammatory cells to mediate MAFLD pathogenesis remains poorly understood. This study aims to investigate the function and mechanism of Hic-5 on hepatic inflammation of MAFLD.
View Article and Find Full Text PDFBiomed Pharmacother
September 2025
Department of Anatomy and Regenerative Biology, Graduate School of Medicine, Osaka Metropolitan University, Osaka, Japan.
Liver fibrosis, which eventually leads to cirrhosis, is characterized by excessive accumulation of type I collagen (COL1A), mainly derived from activated hepatic stellate cells (HSCs). Currently, there is no clinical treatments that can directly address this condition. The objectives of this study were to identify a compound that can suppress HSC activation and elucidate the molecular mechanism underlying its action.
View Article and Find Full Text PDF