For research use only
| Cat No. | ABC-TC3927 |
| Product Type | Mouse Primary Cells |
| Cell Type | Stellate Cell |
| Species | Mouse |
| Growth Conditions | 37 ℃, 5% CO2 |
| Source Organ | Liver |
| Disease | Normal |
| Storage | Liquid Nitrogen |
Mouse Hepatic Stellate Cells reside in liver, store vitamin A, and upon activation drive fibrosis via ECM secretion; ideal for liver injury modeling.
Mouse Hepatic Stellate Cells (MHSCs) are primary mesenchymal cells isolated from mouse liver tissue, specifically from the perisinusoidal space of Disse. Primary MHSCs demonstrate limited proliferative capacity and cryopreserved immediately after isolation. These mesenchymal cells exhibit star-shaped morphology when quiescent and transition to a myofibroblast-like shape upon activation. MHSCs are critical regulators of liver fibrosis, vitamin A storage, and extracellular matrix remodeling. They express markers such as desmin, glial fibrillary acidic protein (GFAP), α-smooth muscle actin (α-SMA), and collagen type I upon activation. Upon liver injury or stress, MHSCs transition into activated myofibroblasts, characterized by increased proliferation and extracellular matrix (ECM) secretion, driving fibrotic responses in conditions like non-alcoholic steatohepatitis and toxin-induced cirrhosis. Their activation is also associated with pro-inflammatory and pro-fibrogenic gene expression, making them an essential model for studying liver injury, repair, and fibrotic progression.
| Product Code | MHSteC |
| Species | Mouse |
| Cat.No | ABC-TC3927 |
| Product Category | Primary Cells |
| Size/Quantity | 1 vial |
| Cell Type | Stellate Cell |
| Growth Mode | Adherent |
| Shipping Info | Dry Ice |
| Growth Conditions | 37 ℃, 5% CO2 |
| Source Organ | Liver |
| Disease | Normal |
| Biosafety Level | 1 |
| Storage | Liquid Nitrogen |
| Product Type | Mouse Primary Cells |
| Quality Control | All cells test negative for mycoplasma, bacteria, yeast, and fungi. |
Mouse Hepatic Stellate Cells offer a robust model system for delving into various facets of liver metabolism and pathophysiology. Their application spans diverse cell-based assays, including toxicity assessment, drug screening, and metabolic studies. They emerge as a crucial resource in the study of liver fibrosis, offering insights that could drive innovative therapeutic strategies for hepatic fibrosis treatment, ultimately aiming to enhance patient outcomes and mitigate the impact of chronic liver injury.
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These cells become activated during liver injury, contributing to fibrosis and scar tissue formation.
In some cases, with appropriate signals, they can return to a less active, quiescent state, though this is limited.
They interact closely with hepatocytes and immune cells, influencing inflammation and tissue remodeling.
Key pathways include TGF-β, PDGF, and Hedgehog signaling, which drive the activation and proliferation of these cells.