For research use only
| Cat No. | ABC-TC3045 |
| Product Type | Mouse Primary Cells |
| Cell Type | Fibroblast |
| Species | B6129SF2/J Mouse |
| Growth Conditions | 37 ℃, 5% CO2 |
| Source Organ | Kidney |
| Disease | Normal |
| Storage | Liquid Nitrogen |
Mouse kidney fibroblasts are isolated from tissue of pathogen-free laboratory mice.
B6129SF2/J Mouse Kidney Fibroblasts are primary cells isolated from the kidney interstitial tissue of B6129SF2/J mice and are suitable for studies of B6129SF2/J kidney fibroblast gene expression under physiological and profibrotic conditions. These fibroblasts exhibit a typical spindle-shaped morphology and adherent growth properties. They play a crucial role in extracellular matrix production, tissue remodeling, and fibrogenesis during renal injury. In vitro, they express mesenchymal markers such as vimentin and α-SMA under profibrotic stimulation. Expression of vimentin and α-SMA is confirmed by immunocytochemistry under profibrotic conditions. These cells provide a biologically relevant model for exploring kidney fibrosis and chronic renal disease. The cells are cryopreserved at early passage, and exhibit limited proliferation capacity. Each lot undergoes rigorous screening and isolation procedures, and is rigorously tested to ensure it is free of contamination from Mycoplasma, Fungi, Yeast, and Bacteria.
| Product Code | B6129SF2/J Mouse Kidney Fibroblasts, B6129SF2J kidney fibroblasts, Mouse kidney fibroblasts B6129SF2/J |
| Species | B6129SF2/J Mouse |
| Cat.No | ABC-TC3045 |
| Product Category | Primary Cells |
| Size/Quantity | 1 vial |
| Cell Type | Fibroblast |
| Growth Mode | Adherent |
| Shipping Info | Dry Ice |
| Growth Conditions | 37 ℃, 5% CO2 |
| Source Organ | Kidney |
| 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. |
B6129SF2/J Mouse Kidney Fibroblasts serve as a critical in vitro model for studying renal fibrosis, stromal-epithelial interactions, and cytokine-mediated signaling pathways in chronic kidney disease. They enable investigation into TGF-β/Smad3 signaling pathways driving collagen deposition, and are used to evaluate antifibrotic therapies, such as FGFR2 inhibitors that attenuate ECM production. These fibroblasts exhibit robust ECM synthesis and myofibroblast differentiation upon stimulation, making them invaluable for screening novel antifibrotic compounds and dissecting fibrogenic mechanisms.
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