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Gene expression profile of cardiac stromal cells from ACM patients in adipogenic medium with and without MB-3 treatment

ABSTRACT: Gene expression profile of cardiac stromal cells from ACM patients in adipogenic medium with and without MB-3 treatment

PROVIDER: PRJNA784092 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17052042.fastq.gz	Fastqsanger.gz
	SRR17052043.fastq.gz	Fastqsanger.gz
	SRR17052044.fastq.gz	Fastqsanger.gz
	SRR17052045.fastq.gz	Fastqsanger.gz
	SRR17052046.fastq.gz	Fastqsanger.gz

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Gene expression profile of cardiac stromal cells from ACM patients in adipogenic medium with and without MB-3 treatment

Project description:Human primary cardiac stromal cells were isolated from arrhythmogenic cardiomyopathy patients and were cultured either in adipogenic medium (ADIPO, A) or in adipogenic medium supplemented with MB-3 (MB-3, M), that is a specific inhibitor of GCN5. The gene expressiona analysis was aimed to investigate the molecular effect of GCN5 inhibition.

2022-07-20 | GSE189657 | GEO

Omics analyses of stromal cells from ACM patients reveal alterations in chromatin organization and mitochondrial homeostasis [Bisulfite-Seq]

Project description:Arrhythmogenic cardiomyopathy (ACM) is a genetic disorder, characterized by ventricular ar-rhythmias, contractile dysfunctions and fibro-adipose replacement of the myocardium. Cardiac mesenchymal stromal cells (CMSC) participate to disease pathogenesis by differentiating towards adipocytes and myofibroblasts. Some altered pathways in ACM are known, but many are yet to be discovered. In order to define changes in the gene expression profiles between ACM- and HC-CMSC, we performed a high throughput Bisulfite-seq on 6 ACM and 6 HC samples. Out of 12466 expressed peaks, 30 resulted differentially expressed. Through enrichment and gene network analyses, we identified differentially regulated pathways, some of which never associated with ACM, including mitochondrial functioning and chromatin organization. Functional validations confirmed that ACM-CMSC exhibited a higher amount of active mitochondria and ROS production, a lower proliferation rate and a more pronounced epicardial-to-mesenchymal transition, compared to controls. In conclusion, ACM-CMSC -omics revealed some additional altered molecular pathways, relevant in the disease pathogenesis, which may constitute novel targets for specific therapies.

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Omics analyses of stromal cells from ACM patients reveal alterations in chromatin organization and mitochondrial homeostasis [RNA-Seq]

Project description:Arrhythmogenic cardiomyopathy (ACM) is a genetic disorder, characterized by ventricular ar-rhythmias, contractile dysfunctions and fibro-adipose replacement of the myocardium. Cardiac mesenchymal stromal cells (CMSC) participate to disease pathogenesis by differentiating towards adipocytes and myofibroblasts. Some altered pathways in ACM are known, but many are yet to be discovered. In order to define changes in the gene expression profiles between ACM- and HC-CMSC, we performed a high throughput RNA-seq on 6 ACM and 6 HC samples. Out of 15031 expressed genes, 529 resulted differentially expressed. Through enrichment and gene network analyses, we identified differentially regulated pathways, some of which never associated with ACM, including mitochondrial functioning and chromatin organization. Functional validations confirmed that ACM-CMSC exhibited a higher amount of active mitochondria and ROS production, a lower proliferation rate and a more pronounced epicardial-to-mesenchymal transition, compared to controls. In conclusion, ACM-CMSC -omics revealed some additional altered molecular pathways, relevant in the disease pathogenesis, which may constitute novel targets for specific therapies.

2024-06-30 | GSE233780 | GEO

Macrophage-derived Spp1 promotes an adipogenic stromal cell population that contributes to intramuscular fat in dystrophic muscle

Project description:In this study we used macrophage-specific ablation combined with single cell transcriptional profiling to uncover the impact of macrophage derived Spp1 on cell-cell interactions in mdx muscles. Ablation of macrophage-specific Spp1 (cKO) correlated with reduction of two novel PDGFR+ stromal cell populations, expressing Lifr+ and Procr+ in cKO muscles. Sorting and transcriptional profiling of Lifr+ and Procr+ stromal cells confirmed that they are enriched in adipogenesis genes and are highly related to fibroadipogenic precursors (FAPS). These adipogenic stromal cells (ASC) were sorted and cultured and shown to be more adipogenic than FAPS, likely due to a more differentiated state. Reduction of ASCs correlated with reduced intramuscular diaphragmatic fat and improved diaphragm function in cKO compared to mdx controls. These data suggest a role for myeloid-derived Spp1 in the differentiation of stromal cells towards an adipogenic fate, leading to accumulation of intramuscular fat in dystrophic muscles.

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Comparing the miRNA transcriptome of FAPs cultured in basal medium (BM) and adipogenic differentiation medium (ADM)

Project description:Comparing the miRNA transcriptome of FAPs cultured in basal medium (BM) and adipogenic differentiation medium (ADM)

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Diverse effects of cyclic AMP variants on osteogenic and adipogenic differentiation of human mesenchymal stromal cells

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Expression profiling of mouse bone marrow skeletal progenitors with osteogenic and adipogenic potential and adipogenic progenitors treated with IFNγ.

Project description:Bone marrow stromal cells (BMSCs) were isolated from the femora and tibiae of irtTA-GBD*-TAg transgenic mice. Using cellular cloning we established skeletal progenitors with unipotent osteogenic and adipogenic properties. Previous RNA-seq analysis of more progenitor types revealed differential expression in members of the Interferon-gamma (IFNγ) signaling pathway. Treatment of adipogenic progenitors with IFNγ inhibited adipogenesis and promoted osteogenesis. RNA-seq analysis of osteogenic, adipogenic and IFNγ treated adipogenic clones revealed factors controlling the osteogenic versus adipogenic commitment of bone marrow skeletal progenitors.

2018-07-02 | GSE114475 | GEO

The arrhythmogenic cardiomyopathy-specific coding and non-coding transcriptome in human cardiac stromal cells

Project description:Background: Arrhythmogenic cardiomyopathy (ACM) is a genetic autosomal disease characterized by abnormal cell-cell adhesion, cardiomyocyte death, progressive fibro-adipose replacement of the myocardium, arrhythmias and sudden death. Several different cell types contribute to the pathogenesis of ACM, including, as recently described, cardiac stromal cells (CStCs). In the present study, we aim to identify ACM-specific expression profiles of human CStCs derived from endomyocardial biopsies of ACM patients and healthy individuals employing TaqMan Low Density Arrays for miRNA expression profiling, and high throughput sequencing for gene expression quantification. Results: We identified 5 miRNAs and 272 genes as significantly differentially expressed. Both the differentially expressed genes as well as the target genes of the ACM-specific miRNAs were found to be enriched in cell adhesion related biological processes. Functional similarity and protein interaction based network analyses performed on the identified deregulated genes, miRNA targets and known ACM-causative genes revealed clusters of highly related genes involved in cell adhesion, extracellular matrix organization, lipid transport and ephrin receptor signaling. Conclusions: We determined for the first time the coding and non-coding transcriptome characteristic of ACM cardiac stromal cells, finding evidence for a potential contribution of miRNAs to ACM pathogenesis or phenotype maintenance. Besides known pathways, we identified also deregulation of genes encoding ephrin receptors and ephrins, thus suggesting a potential involvement of Eph-ephrin signaling in CStCs from ACM hearts.

2018-06-27 | GSE95120 | GEO

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2023-10-06 | GSE214492 | GEO

MEOX2 Regulates Adipogenic Differentiation of Adipose-Derived Stromal Vascular Fractions through PI3K/AKT Signaling Pathway

Project description:The fat tail of sheep is an important organ that has evolved to adapt to extreme environmental conditions. Mesenchyme homeobox 2 (MEOX2) can inhibit adipogenic differentiation of stromal vascular fractions (SVFs) isolated from ovine tail adipose tissue. However, the underlying mechanism through which MEOX2 regulates ovine adipogenesis remains unclear. Therefore, this study aims to employ RNA sequencing (RNA-seq) to explore the downstream genes regulated by MEOX2 during the adipogenic differentiation of ovine SVFs. Based on RNA sequencing, several differentially expressed genes (DEGs) were identified in response to MEOX2 overexpression. The PI3K/AKT signaling pathway was significantly enriched in DEGs, indicating its importance in mediating fat accumulation regulated by MEOX2. Additionally, the PI3K/AKT signaling pathway activation was found to be crucial for ovine SVF adipogenic differentiation. Mechanistically, MEOX2 inhibited the PI3K/AKT pathway. These findings highlight the significance of the PI3K/AKT signaling pathway during ovine SVF adipogenic differentiation. Furthermore, they shed light on the involvement of MEOX2 in this differentiation via the PI3K/AKT pathway. Our findings provide novel insights into the critical role of MEOX2 as an adipogenetic differentiation regulator, potentially enhancing our understanding of ovine fat development and its regulatory processes.

2024-10-01 | GSE266851 | GEO

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