MiRNA profiling in adult rat cardiomyocytes and myocyte-derived progenitor cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus Rattus norvegicus
PROVIDER: GSE24252 | GEO | 2010/09/22
SECONDARY ACCESSION(S): PRJNA132973
REPOSITORIES: GEO
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Project description:TLDA miRNA profiling on purified rat cardiomyocytes (Myo) (Ctl) and myocyte-derived progenitor cells (MDCs) demonstrated significant dedifferentiation of myocytes and identity of stemness, cell cycle progression and proliferation in MDCs after continuous culture in mitogen-rich medium for about 2 weeks. Total RNA was extracted from 3 batches of myocytes or MDCs; 100ug each was subjected to TLDA microRNA profiling after preamplification using ABI's kit. Cardiomyocyte (Myo, Ctl) was used as calibrator sample.
2010-09-22 | E-GEOD-24252 | biostudies-arrayexpress
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2004-08-19 | GSE1055 | 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:We addressed here whether cardiomyocytes generated from CSC differentiation in vitro (iCMs) have a similar pattern of gene expression and undergo a similar transcriptional switch typical of cell cycle exit during adult cardiac myocyte maturation through the activation of known myo-miRs.
2021-09-24 | GSE161081 | GEO
Project description:Rationale: Neonatal mice have the capacity to regenerate their hearts in response to injury, but this potential is lost after the first week of life. The transcriptional changes that underpin mammalian cardiac regeneration have not been fully characterized at the molecular level. Objective: The objectives of our study were to determine if myocytes revert the transcriptional phenotype to a less differentiated state during regeneration and to systematically interrogate the transcriptional data to identify and validate potential regulators of this process. Methods and Results: We derived a core transcriptional signature of injury-induced cardiac myocyte regeneration in mouse by comparing global transcriptional programs in a dynamic model of in vitro and in vivo cardiac myocyte differentiation, in vitro cardiac myocyte explant model, as well as a neonatal heart resection model. The regenerating mouse heart revealed a transcriptional reversion of cardiac myocyte differentiation processes including reactivation of latent developmental programs similar to those observed during de-stabilization of a mature cardiac myocyte phenotype in the explant model. We identified potential upstream regulators of the core network, including interleukin 13 (IL13), which induced cardiac myocyte cell cycle entry and STAT6/STAT3 signaling in vitro. We demonstrate that STAT3/periostin and STAT6 signaling are critical mediators of IL13 signaling in cardiac myocytes. These downstream signaling molecules are also modulated in the regenerating mouse heart. Conclusions: Our work reveals new insights into the transcriptional regulation of mammalian cardiac regeneration and provides the founding circuitry for identifying potential regulators for stimulating heart regeneration. Comparison of transcriptional programs of primary myocardial tissues sampled from neonatal mice and murine hearts undergoing post-injury regeneration, along with in vitro ESC-differentiated cardiomyocytes
2014-12-20 | E-GEOD-64403 | 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 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:Rationale: Neonatal mice have the capacity to regenerate their hearts in response to injury, but this potential is lost after the first week of life. The transcriptional changes that underpin mammalian cardiac regeneration have not been fully characterized at the molecular level. Objective: The objectives of our study were to determine if myocytes revert the transcriptional phenotype to a less differentiated state during regeneration and to systematically interrogate the transcriptional data to identify and validate potential regulators of this process. Methods and Results: We derived a core transcriptional signature of injury-induced cardiac myocyte regeneration in mouse by comparing global transcriptional programs in a dynamic model of in vitro and in vivo cardiac myocyte differentiation, in vitro cardiac myocyte explant model, as well as a neonatal heart resection model. The regenerating mouse heart revealed a transcriptional reversion of cardiac myocyte differentiation processes including reactivation of latent developmental programs similar to those observed during de-stabilization of a mature cardiac myocyte phenotype in the explant model. We identified potential upstream regulators of the core network, including interleukin 13 (IL13), which induced cardiac myocyte cell cycle entry and STAT6/STAT3 signaling in vitro. We demonstrate that STAT3/periostin and STAT6 signaling are critical mediators of IL13 signaling in cardiac myocytes. These downstream signaling molecules are also modulated in the regenerating mouse heart. Conclusions: Our work reveals new insights into the transcriptional regulation of mammalian cardiac regeneration and provides the founding circuitry for identifying potential regulators for stimulating heart regeneration.
2014-12-20 | GSE64403 | 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.
2019-07-02 | GSE49448 | 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.
2016-07-24 | GSE49678 | GEO