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Bulk RNAseq analysis of hypertrophic cardiomyopathy (HCM) hiPSC-derived cardiomyocytes (hiPSC-CMs) and the isogenic control

ABSTRACT: Bulk RNAseq analysis of hypertrophic cardiomyopathy (HCM) hiPSC-derived cardiomyocytes (hiPSC-CMs) and the isogenic control

PROVIDER: PRJNA814293 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18281072_1.fastq.gz	Fastqsanger.gz
	SRR18281072_2.fastq.gz	Fastqsanger.gz
	SRR18281073_1.fastq.gz	Fastqsanger.gz
	SRR18281073_2.fastq.gz	Fastqsanger.gz
	SRR18281074_1.fastq.gz	Fastqsanger.gz

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Bulk RNAseq analysis of hypertrophic cardiomyopathy (HCM) hiPSC-derived cardiomyocytes (hiPSC-CMs) and the isogenic control

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.

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Transcriptome analysis of hiPSC-CMs carrying MYPN mutations

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Project description:In order to investigate the changes of hiPSC-CMS transcriptome after alcohol treatment and whether losartan has an effect on the changes of hiPSC-CM transcriptome after alcohol treatment, RNAseq was performed on hiPSC-CMs treated with 100mM alcohol and 100mM alcohol co-treated with1uM losartan.

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YAP dysregulation triggers hypertrophy by CCN2 secretion and TGFβ uptake in human pluripotent stem cell-derived cardiomyocytes

Project description:Our research has demonstrated the following: (1) Confirmed that MYH7 mutations D239N, H251N, G256E lead to hypercontractility in hiPSC-derived cardiomyocytes (hiPSC-CMs); (2) Increase in YAP’s nuclear localization in both hiPSC-CMs and patient tissue with MYH7 HCM mutations; (3) A correlation between YAP's nuclear localization and enhanced force generation; (4) Nuclear deformation as a mechanism enabling YAP's nuclear entry and activation; (5) Transcriptomic changes resulting from positive and negative modifications in force generation; and (6) A distinctive paracrine hypertrophic signal reliant on cardiomyocyte-cardiac fibroblast crosstalk. Our unique insights to the intricacies of hypertrophic cardiomyopathy phenotypes hold the potential to provide mechanistic clarity, informing potential therapeutic strategies.

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Single-cell sequencing reveals the cardio-protective role of overexpressing Cox7B in hypertrophic cardiomyopathy

Project description:Hypertrophic cardiomyopathy (HCM) is an important cause leading to heart failure. Preserving cardiac function particularly in cardiomyocytes (CMs) is essential for improving prognosis in HCM patients. Therefore, understanding single-cell transcriptome characteristics of CMs in HCM would be indispensable to investigate potential therapeutic targets. We applied single-cell tagged reverse transcription (STRT-seq) approach and obtained 338 CM transcriptomes. The human heart samples were collected from HCM patients who had extended septal myectomy and healthy donors. Our results revealed that in nonfailing HCM heart CMs could be categorized into three subsets: high energy synthesis cluster, high cellular metabolism cluster and intermediate cluster. The expression of mitochondrial and electron transport chain (ETC) was up-regulated in larger-sized CMs from high energy synthesis cluster. Of note, we found the expression of Cytochrome c oxidase subunit 7B (Cox7B), a subunit of Complex IV in ETC was positively correlated with CMs size. Further, after assessing Cox7B expression in HCM patients, we speculated that Cox7B was compensatory up-regulated at early-stage but down-regulated at end-stage of HCM. To test the hypothesis that Cox7B might play a cardioprotective role in the early-stage of HCM, we used adeno associated virus 9 (AAV9) to mediate the expression of Cox7B in pressure overload-induced mice. Mice in vivo data supported that knockdown of Cox7B would accelerate heart failure progression and Cox7B overexpression could restore partial cardiac function in hypertrophy.

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Project description:In this study we performed transcriptome analysis of cardiomyocytes (CMs) derived from two hiPSC lines of patients with V2264M and R1267Q mutations in FLNC gene. hiPSC cell line were obtained from patient’s PBMCs with FLNC mutation using CytoTune-iPS 2.0 Sendai Reprogramming Kit (Thermo Fisher Scientific). Detailed information about iPSC line characterization can be found in hiPSCreg database: (FAMRCi011-A and FAMRCi009). Information about FAMRCi009 is earlier published DOI: 10.1016/j.scr.2021.102640.

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Isogenic Pairs of hiPSC-CMs with Hypertrophic Cardiomyopathy/LVNC-Associated ACTC1 E99K Mutation Unveil Differential Functional Deficits.

Project description:Hypertrophic cardiomyopathy (HCM) is a primary disorder of contractility in heart muscle. To gain mechanistic insight and guide pharmacological rescue, this study models HCM using isogenic pairs of human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) carrying the E99K-ACTC1 cardiac actin mutation. In both 3D engineered heart tissues and 2D monolayers, arrhythmogenesis was evident in all E99K-ACTC1 hiPSC-CMs. Aberrant phenotypes were most common in hiPSC-CMs produced from the heterozygote father. Unexpectedly, pathological phenotypes were less evident in E99K-expressing hiPSC-CMs from the two sons. Mechanistic insight from Ca2+ handling expression studies prompted pharmacological rescue experiments, wherein dual dantroline/ranolazine treatment was most effective. Our data are consistent with E99K mutant protein being a central cause of HCM but the three-way interaction between the primary genetic lesion, background (epi)genetics, and donor patient age may influence the pathogenic phenotype. This illustrates the value of isogenic hiPSC-CMs in genotype-phenotype correlations.

| S-EPMC6235010 | biostudies-literature

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