306-05F

Human Cardiac Fibroblasts: HCF, fetal

• Sinónimos: Cardiac Fibroblasts, Fetal Cardiac Fibroblasts, HCF Cardiac Fibroblasts
• NACRES: NA.81
• UNSPSC Code: 41106514
• Biological source: human heart (normal)
• Growth mode: Adherent
• Morphology: fibroblast
• Relevant disease(s): cardiovascular diseases

Propiedades

• biological source: human heart (normal)
• packaging: pkg of 500,000 cells
• manufacturer/tradename: Cell Applications, Inc
• growth mode: Adherent
• karyotype: 2n = 46
• morphology: fibroblast
• technique(s): cell culture | mammalian: suitable
• relevant disease(s): cardiovascular diseases
• shipped in: dry ice
• storage temp.: −196°C

Descripción

General description

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Cardiac fibroblasts are the most prevalent cell type in the heart, making up 60-70 % of all cells. HCF from Cell Applications, Inc. provide an excellent model system to study many aspects of human heart function and pathophysiology.

HCF has been utilized in a number of research publications, for example to:

• Determine that electrical coupling between cardiomyocytes and fibroblasts is mediated by large-conductance Ca2+-activated K+ channels that can be stimulated by estrogen receptor agonists (Wang, 2006, 2007); and show that antimitogenic effects of estradiol on HCF growth are mediated by cytochromes 1A1/1B1-and catechol-O-methyltransferase-derived metabolites (Dubey, 2005)
• Show that in response to mechanical stretch, cardiac fibroblasts release TGF-β which causes trombomodulin downregulation, increasing the risk of thromboembolic events (Kapur, 2007) and also induces cardiac fibroblast differentiation into myofibroblasts via increased Smad2 and ERK1/2 phosphorylation, that could be stimulated by endothelin-1 and inhibited by Ac-SDKP (Peng, 2010)
• Demonstrate that activation of G protein-coupled receptor kinase-2 (GRK2) prevents normal regulation of collagen synthesis in cardiac fibroblasts mimicking heart failure phenotype (D’Souza, 2011); identify FGF2 signaling pathway as potential target for modulating apoptosis in cardiac pathology (Ma, 2011) and investigate the roles of scleraxis (Bagchi, 2012) and AMPKα1 (Noppe, 2014) in scar formation following myocardial infarction
• Show that the KATP channel opener KMUP-3 preserved cardiac function after myocardial infarction by enhancing the expression of NO synthase and restoring MMP-9/TIMP-1 balance (Liu, 2011)

HCF were also shown to express delayed rectifier IK, Ito, Ca2+-activated K+ current (BKCa), inward-rectifier (Kir-type), and swelling-induced Cl- current (ICl.vol) channels (Yue, 2013).

Application

human heart function, neointimal formation, vascular remodeling, myocardial repair, extracellular maintenance, signaling, toxicology, gene expression, structural support for cardiomycytes, synthesis of extracellular matrix, growth factors and cytokines

Biochem/physiol Actions

Heart

Preparation Note

• 1st passage, >500,000 cells in Basal Medium containing 10% FBS & 10% DMSO
• Can be cultured at least 8 doublings

Please refer to the HCF Culture Protocol.

Other Notes

Basal Medium containing 10% FBS & 10% DMSO

Información de seguridad

• Clase de almacenamiento: 11 - Combustible Solids
• ¿Qué está pasando?: WGK 3
• Punto de inflamación (°F): Not applicable
• Punto de inflamación (°C): Not applicable