Human Cardiac Fibroblasts: HCF, fetal

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 AMPKalpha1 (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).