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RNA-Seq transcriptome profiling of estrogen-related receptor alpha and gamma (ERRa/g) knock out (KO) human iPS cell-derived cardiomyocytes (hiPSC-CMs)

ABSTRACT: Transcriptional regulatory circuits that drive cardiomyocyte maturation are poorly understood. Here we found that in ERRa/g KO hiPSC-CMs, cardiac energy metabolic and cardiac structural transcriptional programs are dysregulated.

ORGANISM(S): Homo sapiens

PROVIDER: GSE165963 | GEO | 2022/02/16

REPOSITORIES: GEO

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Assay for transposase-accessible chromatin sequencing (ATAC-seq) on estrogen-related receptor alpha and gamma (ERRa/g) knock out (KO) human iPS cell-derived cardiomyocytes (hiPSC-CMs)

Project description:To determine the role of estrogen-related receptor alpha and gamma (ERRa/g) on chromatin accessibility, we performed ATAC-seq studies with WT control and ERRa/g KO hiPSC-CMs. We found that ERRa/g activates cardiac chromatin accessibilities in hiPSC-CMs. A subset of the decreased ATAC signals by loss of ERRa/g overlapped ERRg peaks (GSE113760) in hiPSC-CMs, suggesting that ERRg might be directly involved in the activation of cardiac chromatin accessibilities. The motif analysis with decreased ATAC signal by loss of ERRa/g revealed that cardiac-enriched transcription factors such as MEF2 and GATA could cooperate with ERR.

2022-02-16 | GSE165962 | GEO

Genome-wide acetylation of histone 3 at lysine residuce (H3K27ac) deposition in human iPS cell-derived cardiomyocytes (hiPSC-CMs)

Project description:To determine the role of estrogen-related receptor gamma (ERRg) in cardiac myocyte enhancers, we performed ChIP-seq studies with hiPSC-CMs using antibody directed against acetylated histone 3 at lysine residue 27 (H3K27ac), a known active enhancer mark. We found that knocking out ERRg downregulated H3K27ac depositions on several adult cardiac contractile protein and mitochondrial oxidative metabolic genes. These results establish significant roles of ERR to activate cardiac enhancer and promoter activities.

2022-02-16 | GSE165965 | GEO

microRNA profile expression analysis of Human Induced Pluripotent Stem Cell-derived cardiomyocytes (hiPSC-CMs)

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2018-05-01 | GSE111984 | GEO

RNA-Seq transcriptome profiling of human iPS cell-derived cardiomyocytes (hiPSC-CMs) following overexpression (OE) of estrogen-related receptor gamma (ERRg)

Project description:Transcriptional regulatory circuits that drive cardiomyocyte maturation are poorly understood. Human iPS cell-derived cardiomyocytes (hiPSC-CMs) have been shown to have fetal cardiomyocyte features in terms of metabolic gene expression profiles. Here we found that in hiPSC-CMs, overexpression of estrogen-related receptor gamma (ERRg) is sufficient to drive cardiomyocyte metabolic maturation programs including the induction of a number of oxidative mitochondrial metabolic genes.

2022-02-16 | GSE165966 | GEO

RNA-Seq transcriptome profiling of estrogen-related receptor alpha and gamma (ERRa/g) knock out (KO) human iPS cell-derived cardiomyocytes (hiPSC-CMs)

Project description:RNA-Seq transcriptome profiling of estrogen-related receptor alpha and gamma (ERRa/g) knock out (KO) human iPS cell-derived cardiomyocytes (hiPSC-CMs)

| PRJNA698778 | ENA

Maturation of hiPSC-derived cardiomyocytes in tri-cellular cardiac microtissues promotes adult alternative splicing of SCN5A revealing effects of mutations in cardiac disease

Project description:Human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) are used to examine in vitro the effect of mutations in the cardiac sodium channel gene SCN5A, associated with cardiac arrhythmias. Postnatally SCN5A undergoes a fetal-to-adult isoform switch, but hiPSC-CMs in conventional 2-dimensional cultures are fetal-like. This impedes evaluation of mutations in the adult isoform. Here, we derived hiPSC-CMs from a patient carrying compound mutations in the adult SCN5A exon 6B and in exon 4 and generated isogenic corrected lines. In hiPSC-CM 2-dimensional culture, exon 6B mutation did not affect single-cell electrophysiology because of its limited expression. CRISPR/Cas9-mediated excision of the fetal exon 6A with did not promote adult SCN5A expression, rather it impaired the splicing. By maturing hiPSC-CMs in three-dimensional tri-cell type cardiac microtissues, SCN5A underwent isoform switch and revealed the functional effect of exon 6B mutation. Upregulation of the splicing factor MBNL1 in hiPSC-CMs either by culture in microtissues or by overexpression was sufficient to promote exon 6B inclusion. Our results support the ability to study developmentally regulated cardiac genes and postnatal cardiac arrhythmias using hiPSC cardiac cells.

2023-05-03 | GSE180290 | GEO

Altered drug response of recovered human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) from cryopreservation

Project description:We conducted RNA sequcing of the fresh and 1-week recoverd human induced pluripotent stem cell-derived caridomyocytes (hiPSC-CMs) undergo cryopreservation

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Project description:The goal of this study was to identify differential alternative splicing events in RBPMS2-null hiPSC-CMs.

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Project description:To investigate HCM mutation-associated molecular details at the early stage of disease development, we performed bulk RNA-seq analysis at Day 15 of differentiation using RNA isolated from the isogenic control and mutant hiPSC-CMs. We performed pair-end sequencing with >30 million reads per sample with clean read counts of more than 96% for each sample.

2022-07-06 | GSE198258 | GEO

RNA-seq in healthy and SQT1 hiPSC-CMs upon manipulation of miR-365

Project description:Abnormalities of ventricular action potential (AP) cause malignant cardiac arrhythmias and sudden cardiac death. Here, we sought to identify microRNAs (miRNAs) that regulate the human cardiac AP and asked whether their manipulation allows for therapeutic modulation of AP abnormalities. Quantitative analysis of the miRNA targetomes in human cardiac myocytes identified miR-365 as a primary miRNA to regulate repolarizing ion channels. AP recordings in patient-specific induced pluripotent stem cell-derived cardiac myocytes (iPSC-CMs) showed that elevation of miR-365 level significantly prolonged AP duration in hiPSC-CMs derived from a Short-QT syndrome (SQTS) patient, whereas specific inhibition of miR-365 normalized pathologically prolonged AP in Long-QT syndrome (LQTS) iPSC-CMs. Transcriptome analyses in human iPSC-CMs at bulk and single-cell level corroborated the key cardiac repolarizing channels as direct targets of miR-365, together with functionally synergistic regulation of additional AP-regulating genes by this miRNA. Whole-cell patch clamp experiments revealed miR-365-based regulation of repolarizing ionic currents. Finally, refractory period measurements in human myocardial slices substantiated the prolonging effect of miR-365 on AP duration also in adult human myocardial tissue. Our results delineate miR-365 to regulate human cardiac AP duration by targeting key factors of cardiac repolarization.

2021-12-01 | GSE185687 | GEO

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