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$897.00
$897.00
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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
Quality Level
1 of 4
This Item | |||
|---|---|---|---|
| relevant disease(s) cardiovascular diseases | relevant disease(s) cardiovascular diseases | relevant disease(s) - | relevant disease(s) - |
| biological source human heart (normal) | biological source rat heart (Sprague Dawley, neonatal) | biological source human neonatal foreskin or adult skin (normal) | biological source human neonatal foreskin or adult skin (normal) |
| morphology fibroblast | morphology fibroblast | morphology Fibroblast | morphology Fibroblast |
| technique(s) cell culture | mammalian: suitable | technique(s) cell culture | mammalian: suitable | technique(s) cell culture | mammalian: suitable | technique(s) cell culture | mammalian: suitable |
| growth mode Adherent | growth mode Adherent | growth mode Adherent | growth mode Adherent |
| karyotype 2n = 46 | karyotype 2n = 42 | karyotype 2n = 46 | karyotype 2n = 46 |
General description
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
Biochem/physiol Actions
Preparation Note
- 1st passage, >500,000 cells in Basal Medium containing 10% FBS & 10% DMSO
- Can be cultured at least 8 doublings
Other Notes
Disclaimer
Storage Class
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
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Protocols
Culturing HCFs from human heart ventricles involves critical steps for studying cardiac-related conditions.
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