The landscape of accessible chromatin in quiescent cardiac fibroblasts and cardiac fibroblasts activated after myocardial infarction
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ABSTRACT:
PROVIDER: PRJNA772295 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR16474551_1.fastq.gz | Fastqsanger.gz | |||
| SRR16474551_2.fastq.gz | Fastqsanger.gz | |||
| SRR16474552_1.fastq.gz | Fastqsanger.gz | |||
| SRR16474552_2.fastq.gz | Fastqsanger.gz | |||
| SRR16474553_1.fastq.gz | Fastqsanger.gz |
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Project description:In this study, the gene expression profiling and genome-wide accessible chromatin mapping of mouse cardiac fibroblasts isolated from the uninjured myocardium and the infarct at multiple time points corresponding to different differentiation states were performed by RNA sequencing (RNA-seq) and the assay for transposase-accessible chromatin with high-throughput sequencing (ATAC-seq), respectively.
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Project description:After myocardial infarction, the massive death of cardiomyocytes leads to cardiac fibroblast proliferation and myofibroblast differentiation, which contributes to the extracellular matrix remodelling of the infarcted myocardium. We recently found that myofibroblasts further differentiate into matrifibrocytes, a newly identified cardiac fibroblast differentiation state. Cardiac fibroblasts of different states have distinct gene expression profiles closely related to their functions. However, the mechanism responsible for the gene expression changes during these activation and differentiation events is still not clear. In this study, the gene expression profiling and genome-wide accessible chromatin mapping of mouse cardiac fibroblasts isolated from the uninjured myocardium and the infarct at multiple time points corresponding to different differentiation states were performed by RNA sequencing (RNA-seq) and the assay for transposase-accessible chromatin with high-throughput sequencing (ATAC-seq), respectively. ATAC-seq peaks were highly enriched in the promoter area and the distal area where the enhancers are located. A positive correlation was identified between the expression and promoter accessibility for many dynamically expressed genes, even though evidence showed that mechanisms independent of chromatin accessibility may also contribute to the gene expression changes in cardiac fibroblasts after MI. Moreover, motif enrichment analysis and gene regulatory network construction identified transcription factors that possibly contributed to the differential gene expression between cardiac fibroblasts of different states.
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Project description:Cardiac fibroblasts stay relatively quiescent under normal condition. These cells differentiate to myofibroblasts after myocardial infarction (MI), characterized by the expression of contractile proteins and secretion of elevated levels of extracellular matrix proteins, leading to cardiac remodeling. The differentiated myofiroblasts gradually lose most myofibroblast phenotypes but still persist in the infarct area to maintain the tissue structural integrity. We used microarrays to reveal the change in cardiac fibroblast gene expression profile after MI.
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Project description:In response to myocardial infarction (MI), quiescent cardiac fibroblasts differentiate into myofibroblasts mediating tissue repair in the infarcted area. One of the most widely accepted markers of myofibroblast differentiation is the expression of Acta2 which encodes smooth muscle alpha-actin (SMαA) that is assembled into stress fibers. However, the requirement of Acta2/ SMαA in the myofibroblast differentiation of cardiac fibroblasts and its role in post-MI cardiac repair remained largely unknown. To answer these questions, we generated a tamoxifen-inducible cardiac fibroblast-specific Acta2 knockout mouse line. Surprisingly, mice that lacked Acta2 in cardiac fibroblasts had a normal survival rate after MI. Moreover, Acta2 deletion did not affect the function or overall histology of infarcted hearts. No difference was detected in the proliferation, migration, or contractility between WT and Acta2-null cardiac myofibroblasts. It was identified that Acta2-null cardiac myofibroblasts had a normal total filamentous actin level and total actin level. Acta2 deletion caused a significant compensatory increase in the transcription level of non- Acta2 actin isoforms, especially Actg2 and Acta1, 2 other muscle actin isoforms. Moreover, in myofibroblasts the transcription levels of cytoplasmic actin isoforms were significantly higher than those of muscle actin isoforms. In addition, we found that myocardin-related transcription factor-A is critical for myofibroblast differentiation but is not required for the compensatory effects of non-Acta2 isoforms. In conclusion, the deletion of Acta2 does not prevent the myofibroblast differentiation of cardiac fibroblasts or affect the post-MI cardiac repair, and the increased expression and stress fiber formation of non-SMαA actin isoforms and the functional redundancy between actin isoforms are able to compensate for the loss of Acta2 in cardiac myofibroblasts.
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Project description:Cardiac fibrosis occurs in most cardiac diseases, which reduces cardiac muscle compliance, impairs both systolic and diastolic heart function and, ultimately, leads to heart failure. Using unbiased transcriptome profiling in a mouse model of myocardial infarction, we identified a cardiac-fibroblast enriched lncRNA (AK048087) named cardiac fibroblast-associated transcript (Cfast), which is significantly elevated after myocardial infarction. Here, we show that silencing Cfast expression by lentiviral shRNAs resulted in suppression of fibrosis-related gene expression and transdifferentiation of myofibroblasts into cardiac fibroblasts. We performed the RNA-seq profiling in both lentivirus Cfast knockdown and lentivirus scramble group in cardiac fibroblasts. Finally, the transcriptome analysis indicates that genes related to cell differentiation, cell migration, extracellular matrix organization downregulated in Cfast knockdown group.
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Project description:Cardiac fibroblasts were isolated from 3-month old C57BL/6 mice. RNA was prepared from quiescent, serum-starved cardiac fibroblasts in passage 15. A total number of 118654 tags was sequenced. After removal of duplicate ditags and linker-derived sequences 110169 tags remained.
2010-12-01 | GSE25757 | GEO
Project description:Fibrotic scarring drives the progression of heart failure after myocardial infarction (MI). Therefore, the development of specific treatment regimens to counteract fibrosis is of high clinical relevance. The transcription factor SOX9 functions as an important regulator during embryogenesis, but recent data point towards an additional causal role in organ fibrosis. We show here that SOX9 is upregulated in the scar after MI in mice. Fibroblast specific deletion of Sox9 ameliorated MI-induced left ventricular dysfunction, dilatation and myocardial scarring in vivo. Unexpectedly, deletion of Sox9 also potently eliminated persisting leukocyte infiltration of the scar in the chronic phase after MI. RNA-sequencing from the infarct scar revealed that Sox9 deletion in fibroblasts resulted in strongly downregulated expression of genes related to extracellular matrix, proteolysis and inflammation. Importantly, Sox9 deletion in isolated cardiac fibroblasts in vitro similarly affected gene expression as in the cardiac scar and prevented their activation and myofibroblast differentiation. Together, our data demonstrate that fibroblast SOX9 functions as a master regulator of cardiac fibrosis and inflammation and might constitute a novel therapeutic target during MI.
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Project description:Cardiac fibroblasts were isolated from 3-month old C57BL/6 mice. RNA was prepared from quiescent, serum-starved cardiac fibroblasts in passage 15. A total number of 118654 tags was sequenced. After removal of duplicate ditags and linker-derived sequences 110169 tags remained. This GEO Series was created by the GEO staff as part of a cleanup effort to ensure that all GEO Samples are included within a Series entry.
2010-12-01 | E-GEOD-25757 | biostudies-arrayexpress