MiRNA content from human and mouse epicardial extracellular vesicles
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus Homo sapiens
PROVIDER: GSE161630 | GEO | 2020/11/18
REPOSITORIES: GEO
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Project description:Rationale: Epicardium-derived cells (EPDC) are formed in response to myocardial infarction and recapitulate an embryonic program that is likely to participate in cardiac regeneration and remodeling. The existence of atrial counterparts that are potentially involved in atrial remodeling is still elusive. Objective: We have elaborated and validated techniques for the robust isolation and cultivation of atrial and ventricular EPDC from the rat heart and compared their molecular phenotype with human atrial stromal cells obtained from tissue biopsies. Methods and Results: In vitro culture revealed that rat and human cells display a similar morphology, are highly enriched for the epicardial markers WT-1 and Tbx18 throughout in vitro expansion, strongly express the stem/progenitor cell markers CD73, CD90 and, surprisingly the early and late cardiac markers Gata4, Tbx5 and troponin T. In general, these cells display a similar molecular signature - which is different from human MSC - when analyzed by FACS, immunohistochemistry and real time PCR. We also examined the cell surface proteome of human and rat EPDC using cell surface biotinylation combined with nano-liquid chromatography - mass spectrometry. Proteome analysis revealed the presence of 149 overlapping proteins and >200 species specific proteins. These proteins are preferentially involved in cardiac repair and regeneration. Conclusions: This study demonstrates that atrial stromal cells are EPDC suggesting a common epicardial precursor. Cell surface proteome analysis suggests that atrial and ventricular EPDC are likely to play an important role during atrial and ventricular remodeling.
2018-10-19 | PXD005013 | Pride
Project description:Accumulating studies have suggested that epicardial adipose tissue play an important role in the pathogenesis of atrial fibrillation (AF), but few have characterized the underlying mechanism between their interactions. Recent evidence suggested that bioactive molecules secreted from EAT, including exosomes carrying non-coding RNAs, may modulate atrial remodeling. The aim of the present study was to investigate the expression profile of mRNAs and ncRNAs in EAT with AF.
2019-08-07 | GSE135445 | GEO
Project description:By contrast with mammals, adult zebrafish have a high capacity to regenerate damaged or lost myocardium through proliferation of spared cardiomyocytes. The epicardial sheet covering the heart is activated by injury and aids muscle regeneration through paracrine effects and as a multipotent cell source, and has received recent attention as a target in cardiac repair strategies. While it is recognized that epicardium is required for muscle regeneration and itself has high regenerative potential, the extent of cellular heterogeneity within epicardial tissue is largely unexplored. In this study, we performed transcriptome analysis on dozens of epicardial lineage cells purified from zebrafish harboring a transgenic reporter for the pan-epicardial gene tcf21. Hierarchical clustering analysis suggested the presence of at least three epicardial cell subsets defined by expression signatures. We validated many new pan-epicardial and epicardial markers by alternative expression assays. Additionally, we explored the function of the scaffolding protein and main component of caveolae, caveolin-1 (cav1), which was present in each epicardial subset. In BAC transgenic zebrafish, cav1 regulatory sequences drove strong expression in ostensibly all epicardial cells and in coronary vascular endothelial cells. Moreover, cav1 mutant zebrafish generated by genome editing showed grossly normal heart development and adult cardiac anatomy, but displayed profound defects in injury-induced cardiomyocyte proliferation and heart regeneration. Our study defines a new platform for the discovery of epicardial lineage markers, genetic tools, and mechanisms of heart regeneration. Deep sequencing of isolated single epicardial cells
2015-12-15 | E-GEOD-75583 | biostudies-arrayexpress
Project description:Identification of epicardium-enriched genes in the embryonic heart. The epicardium encapsulates the heart and functions as a source of multipotent progenitor cells and paracrine factors essential for cardiac development and repair. Injury of the adult heart results in re-activation of a developmental gene program in the epicardium, but the transcriptional basis of epicardial gene expression has not been delineated. We established a mouse embryonic heart organ culture and gene expression system that facilitated the identification of epicardial enhancers activated during heart development and injury. Epicardial activation of these enhancers depends on a combinatorial transcriptional code centered on CCAAT/enhancer binding protein (C/EBP) transcription factors. Disruption of C/EBP signaling in the adult epicardium reduced injury-induced neutrophil infiltration and improved cardiac function. These findings reveal a transcriptional basis for epicardial activation and heart injury, providing a platform for enhancing cardiac regeneration. Total RNA obtained from lacZ-positive epicardial cells isolated from the E11.5 Tcf21lacZ hearts compared to total dissociated heart cells
2012-11-01 | E-GEOD-41959 | biostudies-arrayexpress
Project description:The overall goal of this study is to determine the transcriptomic consequences of the absence of epicardial-derived cells in the parietal leaflets of the atrioventricular valves as a consequence of epicardial deletion of Sox9.
2024-02-14 | GSE236187 | GEO
Project description:Ischemic heart disease remains the leading cause of mortality and morbidity worldwide despite improved possibilities in medical care. Alongside interventional therapies, such as coronary artery bypass grafting (CABG), adjuvant tissue-engineered and cell-based treatments can provide regenerative improvement. Unfortunately, most of these advanced approaches require multiple lengthy and costly preparation stages without in turn delivering significant clinical benefit.
Here, we investigated the effect of epicardial matrix patch-encased atrial appendage micrografts (AAMs) in a mouse model of myocardial infarction. The matrix-covered AAM patches salvaged the myocardium from infarction-induced functional tissue loss. Fibrosis was attenuated, and site-targeted proteomics revealed AAM patch-activated pathways for angiogenesis and cardiogenesis. The matrix component of the graft further supports functional myocardial recovery by ventricular unloading.
The composite epicardial matrix graft encasing AAM micrografts delivers effects desirable for adjuvant cardiac therapy preserving functional cardiac tissue and restricting fibrosis after myocardial infarction.
2019-07-23 | MSV000084120 | MassIVE
Project description:The analysis showed differences of transcriptomes between primary epicardium explant derived CDCs and primary Epicardial cells directly isolated from the heart epicardium.SB-431542 was an effective TGF-b pathway inhibitor that could obviously inhibit the epicardial cells Epithelial-mesenchymal transition. SB-432542 treatment could produce some epithelial clones in the CDCs,which showed epicardiac specific expression profile, compared with the CDCs.
2022-02-18 | GSE189275 | GEO
Project description:The epicardium is a mesothelial layer covering the myocardium and contributes to different cardiac lineage descendants during cardiogenesis. Fine-tuned balanced signaling defines epicardial specification and regulates cell plasticity and cell-fate decisions of epicardial-derived cells (EPCDs) by epicardial-to-mesenchymal transition (EMT). However, powerful tools to investigate epicardial cell function, including markers with pivotal roles in developmental signaling, are still lacking. Here, we recapitulated embryonic epicardiogenesis using human induced pluripotent stem cells (hiPSCs) and identified type II classical cadherin CDH18 as a novel biomarker defining lineage specification in human developing epicardium. The loss of CDH18 led to the onset of EMT and specific differentiation towards cardiac smooth muscle cells. Furthermore, GATA4 regulated epicardial CDH18 expression. These results demonstrate the production and enrichment of hiPSC-derived epicardial cells via the tracing of CDH18 expression, providing a model for investigating epicardial function in human development and disease and enabling new possibilities for regenerative medicine.
2022-02-18 | GSE165450 | GEO
Project description:Epicardial cells undergo an epithelial-to-mesenchymal transtion (EMT) to generate coronary vascular smooth muscle cells (VSMC) and cardiac fibroblasts. Little is known about the mechanisms regulating EMT or the in vivo signals directing epicardial-derived cell (EPDC) fate. Here, we show that loss of PDGF signaling leads to a disruption in Sox9 expression, and when Sox9 expression was restored in mutant hearts, the EMT defect was rescued. Interestingly, mutants lacking only one of the PDGF genes exhibited a lineage specific requirement for the individual receptors. Loss of PDGFRα resulted in a deficit in cardiac fibroblast formation, while cVSMC development was unperturbed. Conversely, PDGFRβ was required for cVSMC development but not cardiac fibroblast development. Combined, our data demonstrate a novel role for PDGF receptors in epicardial EMT and EPDC development. GSM671723-GSM671724: Total RNA was isolated from E12.5 control and PDGF receptor epicardial knockout hearts using the Trizol reagent. RNA was processed as per manufacturer's instructions (Illumina Gene expression array, Illumina, inc. San Diego, CA, USA) GSM671877-GSM671882: Total RNA was isolated from E12.5 control and PDGF receptor epicardial knockout primary epicardial cultures using the Trizol reagent. RNA was processed as per manufacturer's instructions (Illumina Gene expression array, Illumina, inc. San Diego, CA, USA)
2011-02-28 | E-GEOD-27181 | biostudies-arrayexpress
Project description:Single cell RNA sequencing (scRNA-Seq) is applied to charaterize the pro-epicardial cells (proEpiCs) in mouse pro-epicardial organ (PEO).
2020-04-04 | GSE148040 | GEO