Gene expression profile of induced expandable cardiovascular progenitor cells derived from mouse fibroblasts
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE77375 | GEO | 2016/01/29
SECONDARY ACCESSION(S): PRJNA310182
REPOSITORIES: GEO
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Project description:Cardiovascular progenitor cells (CPCs) can be reprogrammed from somatic fibroblasts by combinations of genes, providing a new avenue for cardiac regenerative therapy. Here we developed a strategy to capture chemically induced CPCs (ciCPCs) during the small molecule-induced cardiac reprogramming of mouse fibroblasts and expand these ciCPCs for a long-term in a chemically defined condition. RNA-seq analysis has been used to compare the expression profile of ciCPCs at early and late passages.
2021-07-01 | GSE159081 | GEO
Project description: Not available
| S-EPMC5826660 | biostudies-literature
Project description:Gene expression profile of chemically induced expandable cardiovascular progenitor cells derived from mouse fibroblasts
| PRJNA667679 | ENA
Project description: Not available
| S-EPMC3678540 | biostudies-literature
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:The regulation of multipotent cardiac progenitor cell (CPC) expansion and subsequent differentiation into cardiomyocytes, smooth muscle, or endothelial cells is a fundamental aspect of basic cardiovascular biology and cardiac regenerative medicine. However, the mechanisms governing these decisions remain unclear. Here, we show that Wnt/β-Catenin signaling, which promotes expansion of CPCs, is negatively regulated by Notch1-mediated control of phosphorylated β-Catenin accumulation within CPCs, and that Notch1 activity in CPCs is required for their differentiation. Notch1 positively, and β-Catenin negatively, regulated expression of the cardiac transcription factors, Isl1, Myocd and Smyd1. Surprisingly, disruption of Isl1, normally expressed transiently in CPCs prior to their differentiation, resulted in expansion of CPCs in vivo and in an embryonic stem (ES) cell system. Furthermore, Isl1 was required for CPC differentiation into cardiomyocyte and smooth muscle cells, but not endothelial cells. These findings reveal a regulatory network controlling CPC expansion and cell fate that involve unanticipated functions of β-Catenin, Notch1 and Isl1 that may be leveraged for regenerative approaches involving CPCs.
2009-05-13 | GSE15232 | GEO
Project description:The transcriptional profiles of cardiac cells derived from murine embryos and from mouse embryonic stem cells (mESCs) have primarily been studied within a cell population. However, the characterization of gene expression in these cells at a single cell level may demonstrate unique variations that are not able to be appreciated as a pool. In this study, we aimed to establish a single cell quantitative PCR platform and perform side-by-side comparison between cardiac progenitors cells (CPCs) and cardiomyocytes (CMs) derived from mESC and mouse embryos. We first generated a reference map for cardiovascular single cells through quantifying lineage-defining genes for CPCs, CMs, smooth muscle cells (SMCs), endothelial cells (EDCs), fibroblasts, and mESCs. This panel was then applied against day 10.5 embryonic heart single cells to demonstrate its ability to identify each endocardial cell and chamber-specific CM. In addition, we compared the gene expression profile of embryo- and mESC-derived CPCs and CMs at different developmental stages and showed that mESC-derived CM is phenotypically similar to embryo-derived CM up to the neonatal stage. Furthermore, we show that single cell expression assay coupled with time-lapse microscopy can resolve the identity and the lineage relationships between progenies of single cultured CPC. With this approach, we found differential propensity for mESC-derived CPCs to become SMCs or CMs, whereas single embryo-derived CPC to become either EDCs or CMs. These results demonstrate that multiplex gene expression analysis in single cells is a powerful tool in examining the unique behavior in individual embryo- or mESC-derived cardiac cells.
2015-01-16 | GSE64938 | GEO
Project description:The regulation of multipotent cardiac progenitor cell (CPC) expansion and subsequent differentiation into cardiomyocytes, smooth muscle, or endothelial cells is a fundamental aspect of basic cardiovascular biology and cardiac regenerative medicine. However, the mechanisms governing these decisions remain unclear. Here, we show that Wnt/β-Catenin signaling, which promotes expansion of CPCs, is negatively regulated by Notch1-mediated control of phosphorylated β-Catenin accumulation within CPCs, and that Notch1 activity in CPCs is required for their differentiation. Notch1 positively, and β-Catenin negatively, regulated expression of the cardiac transcription factors, Isl1, Myocd and Smyd1. Surprisingly, disruption of Isl1, normally expressed transiently in CPCs prior to their differentiation, resulted in expansion of CPCs in vivo and in an embryonic stem (ES) cell system. Furthermore, Isl1 was required for CPC differentiation into cardiomyocyte and smooth muscle cells, but not endothelial cells. These findings reveal a regulatory network controlling CPC expansion and cell fate that involve unanticipated functions of β-Catenin, Notch1 and Isl1 that may be leveraged for regenerative approaches involving CPCs. YFP+ cells marking precardiac mesoderm (Isl1-cre domain) were FACS-sorted (w/wo stabilized Beta-catenin). Their total RNA was amplified with the WT-Ovation Pico RNA Amplification System, fragmented and labeled with the FL-Ovation cDNA Biotin Module V2 (Nugen). The hybridization, staining and scanning of the Affymetrix GeneChips were performed in the Gladstone Genomics Core Lab. Raw data generated from at least three independent experiments were further analyzed by the group of Dr. Ru-Fang Yeh at the Center for Informatics and Molecular Biostatistics, UCSF.
2009-05-13 | E-GEOD-15232 | 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: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