For research use only
| Cat No. | ABC-TC3040 |
| Product Type | Mouse Primary Cells |
| Cell Type | Fibroblast |
| Species | B6129SF2/J Mouse |
| Growth Conditions | 37 ℃, 5% CO2 |
| Source Organ | Heart |
| Disease | Normal |
| Storage | Liquid Nitrogen |
Mouse cardiac fibroblasts are isolated from tissue of pathogen-free laboratory mice.
B6129SF2/J Mouse Cardiac Fibroblasts (CFs) are primary cells isolated from cardiac tissue of B6129SF2/J mice. These cells constitute over 90% of non-myocardial cells in the heart, exhibiting spindle-shaped or polygonal morphology with large oval nuclei and no spontaneous beating. CFs are adherent and proliferate rapidly but have limited passaging capacity. Functionally, CFs synthesize extracellular matrix (ECM) components (e.g., collagen, elastin) to support cardiomyocyte structure and secrete paracrine growth factors during cardiac injury, providing a relevant model for studying B6129SF2/J cardiac cell interaction. Upon activation (e.g., post-myocardial infarction), they differentiate into myofibroblasts expressing α-smooth muscle actin (α-SMA) and collagen I. Expression of α-SMA and collagen I is confirmed by immunocytochemistry. 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 Cardiac Fibroblasts, B6129SF2J cardiac fibroblasts, Mouse cardiac fibroblasts B6129SF2/J |
| Species | B6129SF2/J Mouse |
| Cat.No | ABC-TC3040 |
| 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 | Heart |
| 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. |
These cells serve as an excellent in vitro model for studying cardiac fibrosis, myocardial infarction, and cell–matrix interactions. They are widely used to investigate pro-fibrotic signaling pathways, including TGF-β and angiotensin II responses, enabling the development of antifibrotic therapies and heart failure models. They display robust proliferation in early passages and retain fibroblast markers such as vimentin and DDR2. Their activation and ECM remodeling behavior under stress conditions provide key insights into post-injury cardiac remodeling.
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