2024.05.16
Liver Stellate Cells, or HSCs, are a type of cell within the liver that play a significant role in both physiological and pathological functions. They exhibit irregular shapes such as fusiform, stellate, or polygonal forms. Under normal physiological conditions, HSCs are in a quiescent state, expressing Glial Fibrillary Acidic Protein (GFAP) and Desmin, responsible for maintaining the homeostasis of the extracellular matrix and storing vitamin A in the form of lipid droplets. After liver injury, HSCs become activated by various cytokines into myofibroblast-like cells, which then synthesize and secrete extracellular matrix components to participate in liver damage repair. The activation, proliferation, and transformation of HSCs due to liver injury are crucial steps in the process of liver fibrosis.
Stimulation by multiple cytokines can lead to the activation of HSCs, including Transforming Growth Factor-β1 (TGF-β1), Platelet-Derived Growth Factor (PDGF), Vascular Endothelial Growth Factor (VEGF), and Connective Tissue Growth Factor (CTGF). These stimulating factors trigger the activation of HSCs, induce the synthesis of the extracellular matrix, and increase hepatocyte apoptosis. Among these, TGF-β1 is identified as the most potent pro-fibrotic cytokine discovered to date.
TGF-β1 promotes the formation of liver fibrosis mainly through three mechanisms: 1) It inhibits the degradation of ECM by suppressing Matrix Metalloproteinases (MMPs) and enhancing the activity of Tissue Inhibitors of Metalloproteinases (TIMPs); 2) It induces the formation of myofibroblasts through Epithelial-Mesenchymal Transition (EMT); 3) It stimulates the production of ECM through both Smad-dependent and Smad-independent pathways.
Studies have shown that in mice induced with liver damage by intravenous injection of silica nanoparticles, there is an upregulation of TGF-β1, Smad3, and p-Smad3 protein expression on the 30th and 60th days (as shown in figure A below). The primary effect of TGF-β1 on HSCs is to stimulate the transformation of quiescent HSCs into activated myofibroblasts by upregulating the Notch pathway and the expression of α-Smooth Muscle Actin (α-SMA). Using a receptor blocker like LAP to inhibit the binding of TGF-β1 to its receptor can suppress the elevation of α-SMA.
In addition to inducing liver damage in animals, researchers are currently culturing HSCs in vitro, using TGF-β1 to induce a liver fibrosis model to study and validate related molecular pathways.
MileCell Bio offers Hepatic Stellate Cells with the following advantages:
Good Safety: Negative for mycoplasma and sterility tests, ensuring peace of mind during use.
Worry-Free Compliance: Donor animal tissue sources are clearly compliant.
High Recovery Rate: Cryopreserved cells can achieve a recovery rate of up to 90%, meeting experimental requirements.
High Purity: Immunofluorescence identification with GFAP and Vimentin ensures a purity of up to 90%.
