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Expression data from human myocardial cells, AC16

ABSTRACT: Expression data from human myocardial cells, AC16

PROVIDER: PRJNA593398 | ENA |

REPOSITORIES: ENA

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Expression data from human myocardial cells, AC16

Project description:This study aimed to provide new compelling clues in the PM2.5-induced toxicity and mechanism which order the meaningful bioinformatics evidences for further study on human cardiovascular system. We used microarrays to detail the global programme of gene expression underlying cellularization and identified distinct classes of up-regulated genes after treated with chemical substance

2019-12-05 | GSE141418 | GEO

Expression data from human myocardial cells, AC16

Project description:This study aimed to provide new compelling clues in the PM2.5-induced toxicity and mechanism which order the meaningful bioinformatics evidences for further study on human cardiovascular system. We used microarrays to detail the global program of gene expression underlying cellularisation and identified distinct classes of up-regulated genes after treated with chemical substance.

2017-03-01 | GSE95506 | GEO

RNA sequencing of AC16 and AC16-CAR cells

Project description:RNA sequencing of AC16 and AC16-CAR cells

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HMGN3 ChIP-seq in AC16 cells and Bulk-RNAseq in AC16 cell with and without HMGN3 knockdown

Project description:Chromatin structure plays a central role in regulating gene expression and maintaining cellular identity, yet the structural factors driving these processes in cardiac disease remain poorly defined. To investigate whether these factors can distinguish healthy from diseased cardiac cell populations, we generated a comprehensive list of chromatin structural genes based on an extensive literature review. Applying this list to a published single-cell RNA sequencing (scRNA-seq) dataset from human hearts with and without dilated cardiomyopathy (DCM), we found that chromatin structural gene expression effectively stratified cardiomyocyte and fibroblast populations by disease status. Diseased cardiomyocytes exhibited reduced expression of contractile genes and increased expression of cardiomyopathy markers, while fibroblasts showed enhanced activation signatures. Among these factors, HMGN3 emerged as a candidate of interest, showing consistent downregulation in cardiomyocytes from human patients, as well as in mouse (pressure overload) and pig (myocardial infarction) models of heart failure. Functional studies in AC16 cells revealed that HMGN3 depletion reduced proliferation, increased apoptosis, and decreased active chromatin marks (H3K27ac, H3K4me1), accompanied by increased chromatin compaction. These findings identify HMGN3 as a potential regulator of chromatin architecture in diseased cardiomyocytes, highlight the utility of chromatin structural gene expression in distinguishing pathological cardiac states, and reinforce the role of chromatin organization in shaping the cardiac phenotype. In this dataset, HMGN3 ChIP-seq and Bulk-RNAseq data with and without HMGN3 knockdown were generated using AC16 cells.

2025-12-02 | GSE306626 | GEO

mRNA sequencing of human AC16 cells expressing PCBP1, PCBP2, or both

Project description:To explore potential functional implications of isoform usage shifts, we examined the effect of PCBP1/PCBP2 expression in human AC16 cardiac cells. PCBP1/PCBP2 are KH-domain-containing RNA-binding proteins (RBP) that have been implicated in transcriptional, post-transcriptional and translational regulations. How PCBP1 and PCBP2 are functionally differentiated remains a subject of interest and few reports have outlined their function in cardiac cells. The two paralogs share close homology (~85% identical sequences) and partially overlapping RNA binding targets, suggesting they may form mutually regulatory relationships. Human and mouse PCBP1 sequences share 100.0% identity, whereas human and mouse PCBP2 are identical except in 5 positions; therefore we expressed the human/mouse PCBP1 and human PCBP2 coding sequences in human AC16 cardiac cells. Immunofluorescence imaging confirms broad cytonuclear localization of both paralogs under overexpression. The cells were then subjected to RNA sequencing to determine the effects of PCBP1/2 on gene expression.

2025-07-25 | GSE303619 | GEO

NRF2 upregulation by CDDO-Me protects AC16 human cardiomyocytes against doxorubicin-induced toxicity_1.

Project description:Elucidation of the mechanisms underpinning doxorubicin-induced toxicity in human AC16 cells and the protection afforded by the NRF2 inducer CDDO-Me.

2025-12-12 | GSE313504 | GEO

polysome-IP profiling experiment : Polysomes of untreated or tunicamycin-treated AC16 cells were immunoprecipitated with anti-MRPS15 antibody, followed by RNA sequencing

Project description:Polysomes of untreated (NT) or tunicamycin-treated (TM) human cardiomyocyte AC16 cells were immunoprecipitated (IP MRPS15) with anti-MRPS15 antibody, followed by RNA sequencing. As a control, RNAseq was performed on polysome-associated RNAs of untreated or tunicamycin-treated human cardiomyocyte AC16 cells before immunoprecipitation (input).

2024-04-01 | E-MTAB-13915 | biostudies-arrayexpress

NRF2 upregulation by CDDO-Me protects AC16 human cardiomyocytes against doxorubicin-induced toxicity_2.

Project description:Sequencing study was performed to elucidate the mechanisms underpinning doxorubicin-induced toxicity in human AC16 cells and the protection afforded by the NRF2 inducer CDDO-Me.

2025-12-12 | GSE313552 | GEO

NRF2 upregulation by CDDO-Me protects AC16 human cardiomyocytes against doxorubicin-induced toxicity_3.

2025-12-12 | GSE313503 | GEO

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Project description:Expression data from human myocardial cells, AC16

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