The long noncoding RNA Charme supervises cardiomyocyte maturation by controlling cell differentiation programs in the developing heart
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ABSTRACT:
PROVIDER: PRJNA828100 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18769905_1.fastq.gz | Fastqsanger.gz | |||
| SRR18769905_2.fastq.gz | Fastqsanger.gz | |||
| SRR18769906_1.fastq.gz | Fastqsanger.gz | |||
| SRR18769906_2.fastq.gz | Fastqsanger.gz | |||
| SRR18769907_1.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description: Not available
| S-EPMC10023161 | biostudies-literature
Project description:This SuperSeries is composed of the SubSeries listed below.
2023-03-17 | GSE201027 | GEO
Project description:Charme is a murine long non-coding RNA necessary for the embryonic development of the heart. In vivo Charme knock-out causes prominent alterations of tissue structure, due to cardiac hyperplasia, and leads to the development of cardiac dysfunctions. Although its role in cardiomyocytes has been deeply investigated, no evidence has been collected about its function in other cardiac cell types. Cardiac fibroblasts (CFs) play pivotal roles in the development and homeostatic maintenance of the cardiac tissue. This study investigated the phenotype and function of resident CFs isolated from Charme knockout (CharmeKO) mice, and revealed impaired maturation and functionality. CharmeKO hearts show decreased levels of collagen I content in the extracellular matrix, associated with reduced extracellular matrix-related gene expression and matrix remodelling ability of the CFs. CharmeKO CFs show impaired phenotypic conversion into myofibroblasts and reduced responsiveness to activation stimuli, accompanied by the retention of features proper of unactivated mesenchymal cells. Charme depletion also affects CF paracrine function, determining an impoverishment in cardioprotective cytokines in their secretome, with consequent reduced ability to mediate PI3K/Akt pathway activation in cardiomyocytes and to induce the angiogenic process in endothelial cells. CharmeKO CFs also proved to be less supportive to cardiomyocyte maturation in an in vitro model of cardiac differentiation, thus indicating a potential contribution to the in vivo impairment of cardiomyocyte maturation. Overall, the evidence collected suggests that Charme depletion in the heart impacts CF maturation capacity, leading to their impaired function, which can potentially contribute to the alterations observed in the CharmeKO mice. These findings pave the way to deeper investigations of the intercellular signalling occurring in the heart upon Charme ablation with the aim of identifying how microenvironment homeostasis contributes to cardiomyocyte maturation, and is potentially involved in cardiac diseases.
2026-06-03 | GSE296380 | GEO
Project description:Charme is a murine long non-coding RNA necessary for the embryonic development of the heart. In vivo Charme knock-out causes prominent alterations of tissue structure, due to cardiac hyperplasia, and leads to the development of cardiac dysfunctions. Although its role in cardiomyocytes has been deeply investigated, no evidence has been collected about its function in other cardiac cell types. Cardiac fibroblasts (CFs) play pivotal roles in the development and homeostatic maintenance of the cardiac tissue. This study investigated the phenotype and function of resident CFs isolated from Charme knockout (CharmeKO) mice, and revealed impaired maturation and functionality. CharmeKO hearts show decreased levels of collagen I content in the extracellular matrix, associated with reduced extracellular matrix-related gene expression and matrix remodelling ability of the CFs. CharmeKO CFs show impaired phenotypic conversion into myofibroblasts and reduced responsiveness to activation stimuli, accompanied by the retention of features proper of unactivated mesenchymal cells. Charme depletion also affects CF paracrine function, determining an impoverishment in cardioprotective cytokines in their secretome, with consequent reduced ability to mediate PI3K/Akt pathway activation in cardiomyocytes and to induce the angiogenic process in endothelial cells. CharmeKO CFs also proved to be less supportive to cardiomyocyte maturation in an in vitro model of cardiac differentiation, thus indicating a potential contribution to the in vivo impairment of cardiomyocyte maturation. Overall, the evidence collected suggests that Charme depletion in the heart impacts CF maturation capacity, leading to their impaired function, which can potentially contribute to the alterations observed in the CharmeKO mice. These findings pave the way to deeper investigations of the intercellular signalling occurring in the heart upon Charme ablation with the aim of identifying how microenvironment homeostasis contributes to cardiomyocyte maturation, and is potentially involved in cardiac diseases.
2026-06-03 | GSE296379 | GEO
Project description:The main function of chromatin-associated long non coding RNAs (lncRNA) is to tether specific combinations of regulatory factors to target genomic sites. Here we show the characterization of a conserved lncRNA, Charme, that acts as an architectural scaffold to bring together distantly located genomic loci. The functional knock-down of Charme revealed a direct link between the formation of chromosomal loops and the down-regulation of genes therein contained, which are crucial for the correct control of muscle homeostasis. Notably, several Charme-target genes were previously linked to human cardiomyopathies and Charme deficiency in mice indeed resulted in a very strong cardiac phenotype. Altogether, these data disclose that the chromosomal architecture controlled by Charme is relevant for fine tuning the myogenic programme and for proper tissue homeostasis in vivo.
2018-09-04 | GSE94498 | GEO
Project description:This study establishes the homeodomain only protein, HOPX, as a determinant controlling the molecular switch between cardiomyocyte progenitor and maturation gene programs. This dataset is about time-course CAGE (capped analysis of gene expression) data with genome-wide active transcription footprinting. HOPX CRISPRi cells were differentiated into cardiomyocytes ± DOX and analyzed by CAGE sequencing, among other methods. The study revealed that HOPX interacts with and controls core cardiac networks by regulating the activity of mutually exclusive developmental gene programs.
2022-05-21 | E-MTAB-11719 | biostudies-arrayexpress
Project description:To investigate the role of the lncRNA Charme in cardiac differentiation and physiology, total RNA was collected from CharmeWT and CharmeKO hearts RNA-seq analysis was performed on CharmeWT and CharmeKO postnatal hearts
2023-03-18 | GSE200878 | GEO
Project description:Background: There is a limited capacity to repair damage in the mammalian heart after birth, which is primarily due to the inability of cardiomyocytes to proliferate after birth. This is in contrast to zebrafish and salamander, in which cardiomyocytes retain the ability to proliferate throughout life and can regenerate their heart after significant damage. Recent studies in zebrafish and rodents implicate microRNAs (miRNAs) in the regulation of genes responsible for cardiac cell cycle progression and regeneration, in particular, miR-133a, the miR-15 family, miR-199a and miR-590. However, the significance of these miRNAs and miRNA in general in the regulation of cardiomyocyte proliferation in large mammals, including humans, where the timing of heart development relative to birth is very different than in rodents, is unclear. To determine the involvement of miRNAs in the down-regulation of cardiomyocyte proliferation occurring before birth in large mammals, we investigated miRNA and target gene expression in sheep hearts before and after birth. The experimental approach included targeted transcriptional profiling of miRNA and target mRNA previously identified in rodent studies as well as genome-wide miRNA profiling using microarrays. Results: The cardiac expression of miR-133a increased and its target gene IGF1R decreased with increasing age, reaching their respective maximum and minimum abundance when the majority of ovine cardiomyocytes were quiescent. The expression of the miR-15 family members was variable with age, however, four of their target genes decreased with age. These latter profiles are inconsistent with the direct involvement of this family of miRNA in cardiomyocyte quiescence in late gestation sheep. The expression patterns of ‘pro-proliferative’ miR-199a and miR-590 were also inconsistent with their involvement in cardiomyocyte quiescence. Consequently, miRNA microarray analysis was undertaken, which identified six discrete clusters of miRNA with characteristic developmental profiles. The functions of predicted target genes for the miRNA in four of the six clusters were enriched for aspects of cell division and regulation of cell proliferation suggesting a potential role of these miRNA in regulating cardiomyocyte proliferation. Conclusion: The results of this study show that the expression of miR-133a and one of its target genes is consistent with it being involved in the suppression of cardiomyocyte proliferation, which occurs across the last third of gestation in sheep. The expression patterns of the miR-15 family, miR-199a and miR-590 were inconsistent with direct involvement in the regulation cardiomyocyte proliferation in sheep, despite studies in rodents demonstrating that their manipulation can influence the degree of cardiomyocyte proliferation. miRNA microarray analysis suggests a coordinated and potentially more complex role of multiple miRNA in the regulation of cardiomyocyte quiescence and highlights significant differences between species that may reflect their substantial differences in the timing of this developmental process. RNA, (2 µg) from three heart samples from each of the 91 d (fetus), 141 d (fetus), 5 d (postnatal) and 173 d (postnatal) groups, was used for analysis according to standard procedures. The experimental design included three biological replicates from each of the four normal developmental ages in sheep and thus a total of 12 samples was analyzed.
2015-05-05 | E-GEOD-68496 | biostudies-arrayexpress
Project description:1. Evaluate the diagnostic value of long noncoding RNA (CCAT1) expression by RT-PCR in peripheral blood in colorectal cancer patients versus normal healthy control personal.
2. Evaluate the clinical utility of detecting long noncoding RNA (CCAT1) expression in diagnosis of colorectal cancer patients & its relation to tumor staging.
3. Evaluate the clinical utility of detecting long noncoding RNA (CCAT1) expression in precancerous colorectal diseases.
4. Compare long noncoding RNA (CCAT1) expression with traditional marker; carcinoembryonic antigen (CEA) and Carbohydrate antigen 19-9 (CA19-9) in diagnosis of colorectal cancer.
| 2330122 | ecrin-mdr-crc
Project description:As the fetal heart develops, cardiomyocyte proliferation potential decreases while fatty acid oxidative capacity increases, a highly regulated transition known as cardiac maturation. Small noncoding RNAs, such as microRNAs (miRNAs), contribute to the establishment and control of tissue-specific transcriptional programs. However, small RNA expression dynamics and genome wide miRNA regulatory networks controlling maturation of the human fetal heart remain poorly understood. Transcriptome profiling of small RNAs revealed the temporal expression patterns of miRNA, piRNA, circRNA, snoRNA, snRNA and tRNA in the developing human heart between 8 and 19 weeks of gestation. Our analysis revealed that miRNAs were the most dynamically expressed small RNA species throughout mid-gestation. Cross-referencing differentially expressed miRNAs and mRNAs predicted 6,200 mRNA targets, 2134 of which were upregulated and 4066 downregulated as gestation progresses. Moreover, we found that downregulated targets of upregulated miRNAs predominantly control cell cycle progression, while upregulated targets of downregulated miRNAs are linked to energy sensing and oxidative metabolism. Furthermore, integration of miRNA and mRNA profiles with proteomes and reporter metabolites revealed that proteins encoded in mRNA targets, and their associated metabolites, mediate fatty acid oxidation and are enriched as the heart develops.This study revealed the small RNAome of the maturing human fetal heart. Furthermore, our findings suggest that coordinated activation and repression of miRNA expression throughout mid-gestation is essential to establish a dynamic miRNA-mRNA-protein network that decreases cardiomyocyte proliferation potential while increasing the oxidative capacity of the maturing human fetal heart.
2024-01-26 | PXD044936 | Pride