Primary Cells

B6129SF2/J Mouse Kidney Fibroblasts

  • 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.

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Description

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.

Application

  • 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.

Citation

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