Project description:Analysis of human iPSC-derived cardiomyocytes unstimulated or stimulated with endothelin-1 in the presence of either vehicle (DMSO), Ivermectin, Importazole, IPA-3, or verapamil. Results provide insight into the pathways regulated by the treatments.
Project description:We generated maps of H3K4me1, H3K27ac (enhancers), H3K4me3, Pol II (promoters) and H3K27me3 (repressed chromatin) in the genome of human iPSC-derived cardiomyocytes Differentiation of cardiomyocytes from iPSC followed by ChIP-seq of H3K27ac, H34me1, H327me3, H3K4me3 and PolII
Project description:We generated an interaction map using capture in situ Hi-C in human iPSC-derived cardiomyocytes Differentiation of cardiomyocytes from iPSC followed by capture in situ Hi-C
Project description:Dilated cardiomyopathy (DCM) is the leading cause of heart failure and transplantation worldwide. We used iPSCs to model this disease and compared gene expression change before and after gene therapy of cardiomyocytes derived from DCM-specific iPSCs. We used microarrays to detail the global gene expression of patient specific iPSCs, iPSC-derived cardiomyocytes and its response to gene therapy. Skin fibroblasts and iPSCs derived from a family exhibiting familial dilated cardiomyopathy and H7 human ESCs were subjected to RNA extraction and hybridization on Affymetrix microarrays.Global gene expression pattern were compared and analyzed. Cardiomyocytes derived from iPSCs generated from this DCM family were treated with or without adenoriral Serca2a and subjected to RNA extraction and hybridization on Affymetrix microarrays. Global gene expression pattern were compared and analyzed.
Project description:The human iPSC line H19101 was differentiated in vitro into cardiomyocytes using a 20-day differentiation protocol (Burridge et al. 2014 PMID 24930130 and Montefiori et al 2018 PMID 29988018 ). 50,000 cardiomyocytes were used in each ATAC-seq experiment. 8 replicates were pooled to obtain the final peak file.