Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

8 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression data from patient iPSC

ABSTRACT: Baseline gene expression of patient dermal fibroblasts derived iPSCs generated by lentiviral Yamanaka 4 factors. We used microarrays to detail the global gene expression of Hypertrophic cardiomyopathy (HCM) patient specific iPSCs. Compare the global gene expression of iPSCs with hESCs and fibroblasts

ORGANISM(S): Homo sapiens

SUBMITTER: Leng Han

PROVIDER: E-GEOD-35229 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Expression data from patient iPSC

Project description:Baseline gene expression of patient dermal fibroblasts derived iPSCs generated by lentiviral Yamanaka 4 factors. We used microarrays to detail the global gene expression of Hypertrophic cardiomyopathy (HCM) patient specific iPSCs.

2012-04-01 | GSE35229 | GEO

Expression data from patient iPSC and iPSC-derived cardiomyocytes

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.

2012-02-01 | E-GEOD-35108 | biostudies-arrayexpress

Transcriptomic profileing of iPSC-derived engineered cardiac tissue in which cMyBP-C have been ablated in the heterozygous and homozygous states on an isogenic background

Project description:Truncation mutations in cardiac myosin binding protein C (cMyBP-C), are common causes of hypertrophic cardiomyopathy (HCM). Heterozygous carriers present with classical HCM, while homozygous carriers present with early onset HCM that rapidly progress to heart failure. We used CRISPR-Cas9 to introduce heterozygous (cMyBP-C+/-) and homozygous (cMyBP-C-/-) frame-shift mutations into MYBPC3 in human iPSCs. Cardiomyocytes derived from these isogenic lines were used to generate engineered cardiac tissue constructs (ECTs). RNAseq analysis on 14 day old ECTs revealed enrichment of differentially expressed hypertrophic, sarcomeric, Ca2+-handling and metabolic genes in cMyBP-C+/- and cMyBP-C-/- ECTs.

2023-02-23 | GSE224129 | GEO

miRNA expression profiles in the serum of cats with hypertrophic cardiomyopathy compared to healthy cats

Project description:MicroRNAs negatively regulate gene expression and may serve as biomarkers for human cardiomyopathy. In the domestic cat, hypertrophic cardiomyopathy (HCM) represents the most common primary cardiomyopathy. In humans, the etiology of HCM is linked to mutations in genes of contractile muscle proteins, while in cats a clear proof for causal mutations is missing. The etiology of feline HCM is uncertain. Diagnosis is made by heart ultrasound examination and measuring the serum level of N-terminal pro B-type natriuretic peptide. The purpose of this study was to investigate whether microRNA profiles in the serum of cats with HCM are different from the profiles of healthy cats and whether specific miRNAs can be detected to serve as potential biomarkers for feline HCM or may help in understanding the etiology of this disease Blood was drawn from two groups of cats: 12 healthy cats and 11 cats suffering from hypertrophic cardiomyopathy. After clotting, samples were centrifuged and total mRNA was extracted from serum. These 23 serum samples were analyzed and the groups were compared

2015-07-22 | E-GEOD-49427 | biostudies-arrayexpress

Transcription profiling by array of human induced pluripotent stem cells generated with Yamanaka factors and miR-302 cluster

Project description:Baseline gene expression of adipose stem cell derived iPSCs generated by lentiviral Yamanaka 4 factors. We used microarrays to analyze the global gene expression of hACS derived iPSCs with KMOS and KMOS+miR-302. Compare the global gene expression of iPSCs with hESCs and adipose stem cells.

2012-05-31 | E-GEOD-37896 | biostudies-arrayexpress

Human Obstructive and Non-obstructive Hypertrophic Cardiomyopathy Disease Mechanisms

Project description:To understand the interplay between cardiomyocyte and nonmyocyte cell types in human obstructive and non-obstructive hypertrophic cardiomyopathy, single nuclei RNA-sequencing was performed on 2 unused donor hearts, 1 obstructive HCM specimen, and 6 non-obstructive HCM specimens.

2022-01-01 | GSE181764 | GEO

Circular RNA circZFPM2 regulates cardiomyocyte hypertrophy and survival

Project description:Hypertrophic cardiomyopathy (HCM) constitutes the most common genetic cardiac disorder. However, current pharmacotherapeutics are mainly symptomatic and only partially address underlying molecular mechanisms. Circular RNAs (circRNAs) are a recently discovered class of non-coding RNAs and emerged as specific and powerful regulators of cellular functions. By performing global circRNA-specific next generation sequencing in cardiac tissue of patients with hypertrophic cardiomyopathy compared to healthy donors, we identified circZFPM2 (hsa_circ_0003380. CircZFPM2, which derives from the ZFPM2 locus, is a highly conserved regulatory circRNA that is strongly induced in HCM tissue. In vitro loss-of-function experiments were performed in neonatal rat cardiomyocytes, human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs), and HCM-patient-derived hiPSC-CMs. A knockdown of circZFPM2 was found to induce cardiomyocyte hypertrophy and compromise mitochondrial respiration, leading to an increased production of reactive oxygen species and apoptosis. In contrast, delivery of recombinant circZFPM2, packaged in lipid-nanoparticles or using AAV-based overexpression, rescued cardiomyocyte hypertrophic gene expression and promoted cell survival. Additionally, HCM-derived cardiac organoids exhibited improved contractility upon CM-specific overexpression of circZFPM2. Multi-Omics analysis further promoted our hypothesis, showing beneficial effects of circZFPM2 on cardiac contractility and mitochondrial function. Collectively, our data highlight that circZFPM2 serves as a promising target for the treatment of cardiac hypertrophy including HCM.

2024-04-25 | GSE261129 | GEO

Heat Shock Proteins and Small Nucleolar RNAs are Dysregulated in a Drosophila Model for Feline Hypertrophic Cardiomyopathy

Project description:We report the application of RNA-sequencing technology for high-throughput profiling of Drosophila that express clinical variants of feline-MyBPC3 associated with Hypertrophic Cardiomyopathy (HCM).

2020-12-04 | GSE141574 | GEO

Altered Intercellular Communication and Extracellular Matrix Signaling as a Disease Mechanism in Human Hypertrophic Cardiomyopathy

Project description:To understand the interplay between cardiomyocyte and nonmyocyte cell types in human hypertrophic cardiomyopathy, single nuclei RNA-sequencing was performed on 9 myectomy specimens from HCM patients

2021-05-20 | GSE174691 | GEO

Isogenic human pluripotent stem cell disease models reveal actin binding Rho activating protein deficiency underlies the cardiac troponin T DK210 mutation-induced familial dilated cardiomyopathy II

Project description:Different single mutations on the same sarcomeric gene often cause distinct cardiomyopathy phenotypes as dilated (DCM) or hypertrophic cardiomyopathy (HCM). The key factors involved in this disease divergence is unknown and could be key for disease intervention.We generated isogenic familial DCM and HCM disease-specific human embryonic stem cells (hESCs) carrying the cTnT-DK210 and -DE160 mutation, respectively. Whole transcriptomic RNA-sequencing was used to identify the key gene involved in the earliest disease divergence of cTnT-DK210 caused DCM and cTnT-DE160 caused HCM. Results provide insight into the new molecular mechanisms underlying familial dilated cardiomyopathy.

2021-10-01 | GSE154097 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data