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Species | Human |
Cat.No | ABC-TC075G |
Quality Control | All cells test negative for mycoplasma, bacteria, yeast, and fungi. |
Product Category | Primary Cells |
Size/Quantity | 1 vial |
Cell Type | Fibroblast |
Shipping Info | Dry Ice |
Growth Conditions | 37 ℃, 5% CO2 |
Source Organ | Lung |
Disease | COPD |
Biosafety Level | 1 |
Storage | Liquid Nitrogen |
Product Type | Pulmonary Cells |
AcceGen provides Diseased Human Lung Fibroblasts isolated from adult COPD donors, which are cryopreserved at passage 2 with 0.5 million cells in each vial. Cells are negative for von Willebrand factor VIII, cytokeratins 18 and 19, and alpha smooth muscle actin. HIV-1, hepatitis B and hepatitis C are not detected for all donors.
When you publish your research, please cite our product as “AcceGen Biotech Cat.# XXX-0000”. In return, we’ll give you a $100 coupon. Simply click here and submit your paper’s PubMed ID (PMID).
For research use only
Diseased Human Lung Fibroblasts are fibroblasts that have been isolated from the lungs of patients with chronic lung diseases, such as Chronic Obstructive Pulmonary Disease (COPD). These cells play a crucial role in the remodeling and fibrosis of lung tissue associated with COPD.
In COPD, fibroblasts contribute to the pathological remodeling of lung tissue, leading to fibrosis, thickening of the airway walls, and reduced lung function. They are involved in the production of extracellular matrix proteins, which can accumulate and disrupt normal lung architecture.
Diseased lung fibroblasts in COPD patients often exhibit an altered phenotype, including increased proliferation, resistance to apoptosis, and enhanced production of extracellular matrix components. These changes contribute to the pathological features of COPD, such as fibrosis and airway obstruction.
Diseased lung fibroblasts are used in research to study the mechanisms of tissue remodeling and fibrosis in COPD, to identify potential therapeutic targets, and to test the effects of drugs that could inhibit fibroblast activity or reverse fibrosis.
These fibroblasts contribute to the progression of COPD by promoting the deposition of extracellular matrix components, leading to fibrosis and stiffening of lung tissue. This results in airway narrowing and reduced lung function, which are hallmarks of COPD.