For research use only
| Cat No. | ABC-TC3203 |
| Product Type | Mouse Primary Cells |
| Cell Type | Fibroblast |
| Species | C57BL/6 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.
C57BL/6 Mouse Kidney Fibroblasts are primary cells isolated from the kidney tissue of pathogen-free laboratory mice. These mouse fibroblasts reside in the renal interstitium, especially within the tubulointerstitial compartment surrounding renal tubules. Following primary culture, these cells are cryopreserved. The cells play a crucial role in mediating extracellular matrix remodeling, inflammatory cytokine secretion, and immune cell recruitment via chemokine signaling. Studies have demonstrated their critical involvement in chronic kidney disease, diabetic nephropathy, and obstructive nephropathy. Phenotypic characterization confirms expression of fibroblast markers CD90.2 (Thy1.2), PDGFR-β, and FSP-1 (S100A4). Repeated freezing and thawing should be avoided during culture. The cells undergo rigorous screening and isolation procedures, and are rigorously tested to ensure they are free of contamination from Mycoplasma, Fungi, Yeast, and Bacteria.
| Product Code | C57BL/6 Mouse Kidney Fibroblasts, Mouse Kidney Fibroblasts, Kidney Fibroblasts, Fibroblasts, FibCs, C57BL/6 Kidney Fibroblasts |
| Species | C57BL/6 Mouse |
| Cat.No | ABC-TC3203 |
| 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. |
C57BL/6 Mouse Kidney Fibroblasts can be used as an in vitro model to study the pathogenesis of renal fibrotic disorders in disease conditions such as chronic kidney disease (CKD) and diabetic nephropathy. Researchers can investigate critical pathological mechanisms including TGF-β-mediated collagen accumulation in chronic kidney disease, hyperglycemia-induced fibronectin deposition in diabetic nephropathy, and progressive tubulointerstitial scarring in obstructive uropathy.
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