Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA385605 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5512800_1.fastq.gz | Fastqsanger.gz | |||
| SRR5512800_2.fastq.gz | Fastqsanger.gz | |||
| SRR5512791_1.fastq.gz | Fastqsanger.gz | |||
| SRR5512791_2.fastq.gz | Fastqsanger.gz | |||
| SRR5512801_1.fastq.gz | Fastqsanger.gz |
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Project description:High throughput single-cell whole transcriptome analysis of induced cardiomyocytes during direct cardiac reprogramming [RNA-seq]
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Project description:Analysis of induced cardiomyocytes during direct cardiac reprogramming
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Project description:The reprogramming of fibroblast cells to induced pluripotent stem (iPS) cells raises the possibility that a somatic cell could be reprogrammed to an alternative differentiated fate without first becoming a stem/progenitor cell. A large pool of fibroblast cells exists in the post-natal heart, yet no single “master regulator” of direct cardiac reprogramming has been identified. Here, we report that a combination of three developmental transcription factors (i.e., Gata4, Mef2c and Tbx5) rapidly and efficiently reprogrammed post-natal cardiac or tail-tip fibroblasts directly into differentiated cardiomyocyte-like cells. Induced cardiomyocytes expressed cardiac-specific markers, had a global gene expression profile similar to cardiomyocytes, and contracted spontaneously. Fibroblast cells transplanted into mouse hearts one day after transduction of the three factors also differentiated into cardiomyocyte-like cells. These findings demonstrate that functional cardiomyocytes can be directly reprogrammed from differentiated somatic cells by defined factors. Reprogramming of endogenous or explanted fibroblast cells might provide a source of cardiomyocytes for regenerative approaches.
2010-06-12 | GSE22292 | GEO
Project description:Adult cardioyocytes undergo remarkable dedifferentiation and cell cycle reprogramming/reentery when cultured in mitogen-rich medium, continuously, and give rise to cardiac progenitor cells (CPCs). Using microfluidic device for single-cell capture and whole-transcriptomic amplification, we analyze the whole-genome transcriptomic profile in adult mouse cardiomyocytes (Ctl) and in their derived CPCs, and validate the gene expression by single-cell PCR and PCR array. Using two platforms for DNA methylation profiling: NimbleGen DNA methylation array and CHARM array, the whole-genome DNA methylation profile in myocytes (Ctl) and CPCs were compared and their regulations in relationship to the transcriptomics profile were analyzed. The results demonstrated remarkable molecular reprogramming pertaining to dedifferentiation, loss of cardiac contractile, structure, and function molecules, and reactivation of cell cycle and proliferation genes, significant changes in metabolisms. The reduction of cardiac function and structure genes are highly related to their hypermethylation of the promoter regions. GO and Pathway enrichment analysis revealed distinct coordianted transcriptomic and epigenetic regulation in the CPCs derived from cardiomyocytes. Mouse single cardiomyocytes (Ctl) and their derievd single CPCs were captured using microfluidic deviced and cDNA synthesized and amplified and labelled using NuGENE kits, and regular Affymetrix hybridization and wash protocols were used to process the mouse whole-genome array GeneChip 430 2.0.
2016-07-24 | E-GEOD-49448 | biostudies-arrayexpress
Project description:Direct cardiac reprogramming converts fibroblasts into induced cardiomyocytes (iCMs) with the minimal combination of transcription factors, Gata4 (G), Mef2c (M), and Tbx5 (T). However, the induction of functional mature iCMs is inefficient and the mechanisms remain elusive. Mef2c is a central transcription factor in direct cardiac reprogramming. We investigated the effect of Mef2c isoforms(M1, M2, M6) and transcriptional activity (M2TAD) on cardiac reprogramming on cardiac reprogramming. Then, we found that the active form of Mef2c evoked epigenetic remodeling cooperating with p300 and promoted the maturation of iCMs.
2023-06-13 | GSE196293 | GEO
Project description:Direct conversion of cardiac fibroblast into functional induced cardiomyocytes by forced expression of three cardiac transcription factors, Mef2c, Gata4, and Tbx5, holds great promise for regenerative medicine. Cardiac reprogramming consists of waves of transcription remodeling events, including the fast acquisition of cardiac program and the gradual loss of fibroblast program. However, how this transcription remodeling was driven by the upstream chromatin landscape is still unclear. In this study, we performed single-cell ATAC-seq on Day 3 cardiac reprogramming cells and unveiled networks of transcription factors (TFs) playing a pivotal role in the shift of chromatin accessibility during the early stage of cardiac reprogramming. Moreover, integration analysis of scRNA-seq and scATAC-seq lead to the identification of active TFs function as barriers to cardiac reprogramming.
2021-09-05 | GSE171525 | GEO
Project description:Adult cardioyocytes undergo remarkable dedifferentiation and cell cycle reprogramming/reentery when cultured in mitogen-rich medium, continuously, and give rise to cardiac progenitor cells (CPCs). Using microfluidic device for single-cell capture and whole-transcriptomic amplification, we analyze the whole-genome transcriptomic profile in adult mouse cardiomyocytes (Ctl) and in their derived CPCs, and validate the gene expression by single-cell PCR and PCR array. Using two platforms for DNA methylation profiling: NimbleGen DNA methylation array and CHARM array, the whole-genome DNA methylation profile in myocytes (Ctl) and CPCs were compared and their regulations in relationship to the transcriptomics profile were analyzed. The results demonstrated remarkable molecular reprogramming pertaining to dedifferentiation, loss of cardiac contractile, structure, and fucntion molecules, and reactivation of cell cycle and proliferation genes, significant changes in metabolisms. The reduction of cardiac function and structure genes are highly related to their hypermethylation of the promoter regions. GO and Pathway enrichment analysis revealed distinct coordianted transcriptomic and epigenetic regulation in the CPCs derived from cardiomyocytes. Genomic DNA isolated from adult mouse cardiomyocytes (Ctl) or cardiomyocyte-derived progenitor cells (CPCs) was subjected to digestion by methylcytosine-sensitive enzyme McrBC, and subsequently purification and amplification, labeling and hybridization to the NimbleGen 3x720K DNA methylation Promoter array, according to NimbleGen protocol. Percentage methylation, hypermethylation or hypomethylation, and peak enrichment were assessed using CHARM protocol.
2016-07-24 | E-GEOD-49678 | biostudies-arrayexpress
Project description:Adult cardioyocytes undergo remarkable dedifferentiation and cell cycle reprogramming/reentery when cultured in mitogen-rich medium, continuously, and give rise to cardiac progenitor cells (CPCs). Using microfluidic device for single-cell capture and whole-transcriptomic amplification, we analyze the whole-genome transcriptomic profile in adult mouse cardiomyocytes (Ctl) and in their derived CPCs, and validate the gene expression by single-cell PCR and PCR array. Using two platforms for DNA methylation profiling: NimbleGen DNA methylation array and CHARM array, the whole-genome DNA methylation profile in myocytes (Ctl) and CPCs were compared and their regulations in relationship to the transcriptomics profile were analyzed. The results demonstrated remarkable molecular reprogramming pertaining to dedifferentiation, loss of cardiac contractile, structure, and function molecules, and reactivation of cell cycle and proliferation genes, significant changes in metabolisms. The reduction of cardiac function and structure genes are highly related to their hypermethylation of the promoter regions. GO and Pathway enrichment analysis revealed distinct coordianted transcriptomic and epigenetic regulation in the CPCs derived from cardiomyocytes. Genomic DNA isolated from adult mouse cardiomyocytes (Ctl) or cardiomyocyte-derived progenitor cells (CPCs) was subjected to digestion by methylcytosine-sensitive enzyme McrBC, and subsequently purification and amplification, labeling and hybridization according to NimbleGen protocol. Percentage methylation, hypermethylation or hypomethylation, and peak enrichment were assessed using CHARM protocol.
2016-07-24 | E-GEOD-49676 | biostudies-arrayexpress
Project description:Direct reprogramming has revolutionized the fields of stem cell biology and regenerative medicine. Direct reprogramming makes it possible to interconvert somatic cell fates without intermediary pluripotency. Although studies have identified different transcription factor (TF) cocktails that can reprogram fibroblasts into different cell types, the common mechanisms governing how reprogramming cells undergo transcriptome and epigenome remodeling (i.e. regulatome remodeling) have not been investigated. Here, by characterizing early changes in the regulatome of three different types of direct reprogramming – induced neurons, induced hepatocytes, and induce cardiomyocytes – we identified two non-cocktail TFs, Tead4 and Atf7, that co-operate with reprogramming TFs to regulate target cell-type specific gene expression. Additionally, by identifying shared pro-cardiac features of iN and iCM reprogramming, we demonstrate Ascl1’s cross-lineage potential to induce highly efficient iCM reprogramming in a two-factor cocktail with Mef2c (A+M). Single-cell multi-omics showed that A+M reprogramming terminates in a more mature iCM phenotype than MGT. Finally, through ChIP-seq and RNA-seq, we find that Mef2c drives the shift in Ascl1 binding away from neuronal genes towards cardiac gene, guiding their co-operative epigenetic and transcription activities. These findings demonstrate the existence of common regulators of different direct reprogramming process and argue against the premise that TFs are lineage specific – the basic premise used to develop direct reprogramming approaches.
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