Rattus norvegicus
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PROVIDER: PRJNA162385 | ENA |
REPOSITORIES: ENA
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Project description:Cardiac fibrosis is a detrimental pathophysiological state involved in a number of cardiovascular diseases. Myofibroblasts mediate fibrosis by excessive remodeling of the extracellular matrix, which ultimately leads to tissue stiffness and impaired heart performance. Recently, it was shown that a substantial fraction of cardiac myofibroblasts may originate from the epicardium through Epithelial-to-Mesenchymal Transition (EMT). We have developed a cellular model of EMT in which adult murine epicardium-derived cells are differentiated into myofibroblast-like cells in the presence of Interleukin-1beta, Tumor Necrosis Factor-alpha, or Transforming Growth Factor-beta. Using this model of EMT, the microRNAome was assessed by microRNA (miRNA) arrays. Subsequently, expression levels of differentially expressed miRNAs were validated by qPCR. These miRNAs were targeted by transfecting epicardium-derived cells with anti- or pre-miRs prior to EMT initiation. The ability of the anti- or pre-miRs to inhibit EMT was assessed on a number of phenotypic markers. In this study we have identified a number of miRNAs that potentially play an intrinsic role in cardiac EMT. We speculate that by targeting those miRNA, the onset and long-term progression of cardiac fibrosis can be substantially reduced. Epicardial mesothelial cells were isolated and expanded from the epicardium of adult rats (8-10 weeks). Epithelial-to-mesenchymal Transition was induced by 10 ng/mL Interleukin-1beta, Tumor Necrosis Factor-alpha, or Transforming Growth Factor-beta1 for 48h. The assocciated differential microRNA expressions relative to a control treatment was computed by microRNA arrays. The experiment was conducted on biological quadruplicates for the control treatment and biological triplicates for cytokine treatments.
2012-04-26 | E-GEOD-37627 | biostudies-arrayexpress
Project description:CCBE1 is a secreted extracellular matrix protein expressed by epicardial cells but its role during epicardial development was still unknown.Using a Ccbe1 knockout (KO) mouse model, we observed that loss of CCBE1 leads to congenital heart defects including thinner and hyper-trabeculated ventricular myocardium. In addition, Ccbe1 mutant hearts displayed reduced proliferation of cardiomyocyte and epicardial cells. RNA-seq data of CCBE1 KO and WT murine hearts indicated deregulation of genes associated with development and morphogenesis including the epithelial-to-mesenchymal transition.
2022-10-23 | E-MTAB-12217 | biostudies-arrayexpress
Project description:Cardiovascular disease (CVD) is one of the leading causes of mortality worldwide, and frequently leads to massive heart injury and the loss of billions of cardiac muscle cells and associated vasculature. Critical work in the last two decades demonstrated that these lost cells can be partially regenerated by the epicardium, the outermost mesothelial layer of the heart, in a process that highly recapitulates its role in heart development. Upon cardiac injury, mature epicardial cells activate and undergo an epithelial-mesenchymal transition (EMT) to form epicardial-derived progenitor cells (EpiPCs), multipotent progenitors that can differentiate into several important cardiac lineages, including cardiomyocytes and vascular cells. In mammals, this process alone is insufficient for significant regeneration, but it may be possible to prime it by administering specific reprogramming factors, leading to enhanced EpiPC function. Here, we compared changes in gene expression induced by oxytocin in epicardial cells to determine potential pro-regenerative effects.
2022-09-01 | GSE199427 | GEO
Project description:Adult zebrafish regenerate heart muscle after severe cardiac damage without significant scarring. The epicardium, a mesothelial cell sheet covering the vetebrate heart, is activated by injury and supports muscle regeneration through paracrine effects and as a source of multipotent cells. The understudied cellular heterogeneity of the adult epicardium during heart regeneration has constrained the effort in mobilizing the epicardium for heart repair. To dissect epicardial cell states and the underlying mechanisms that lead to successful heart regeneration in zebrafish, we performed single-cell RNA-sequencing of isolated epicardial cells from the regenerating adult heart and revealed their dynamic cellular heterogeneity. We defined the epithelial and mesenchymal layers of the epicardium and identified a transiently activated epicardial progenitor cell (aEPC) subpopulation that expresses aldh1a2, ptx3a, col12a1b and marcksb. Upon heart amputation injury, aEPCs emerge from the existing epicardial cells, migrate to enclose the wound, and disappear as regeneration progresses. Genetic lineage tracing combined with modified RNA labelling confirmed an epithelial-mesenchymal transition (EMT) process of aEPCs and their differentiations to pdgfrb+ mural cells and pdgfra+hapln1a+ mesenchymal fibroblast-like cells that support heart regeneration. Genetic ablation of aEPCs blocked wound closure of the injured ventricle, suppressed cardiomyocyte proliferation, and disrupted heart regeneration. Our findings define a transient progenitor state of the adult epicardium that is an indispensable driver of zebrafish heart regeneration and identified ptx3a as a regeneration-specific non-ontogenetic regulator of the epicardium.
2022-11-22 | GSE202836 | 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:The embryonic epicardium provides a source of multipotent progenitors for cardiac lineages, including pericytes, fibroblasts and smooth muscle cells. However, it remains unclear if the epicardium comprises of heterogeneous progenitors or if epicardial cells are multipotent. Using scRNA-seq, we analysed the expression profile of epicardial and epicardial-derived cells at E15.5 and found no evidence of discrete epicardial sub-compartments. Our findings also support the notion that epicardial fate is specified after epithelial-mesenchymal transition, not pre-determined.
2020-04-30 | GSE145832 | GEO
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:Long-term peritoneal dialysis is associated with progressive fibrosis of the peritoneum. Epithelial-mesenchymal transition (EMT) of mesothelial cells is an important mechanism involved in peritoneal fibrosis, and TGF-b1 is considered central in this process. We conducted network-based integrated analysis of transcriptomic data to systemically characterize the molecular signature of TGF-b1-stimulated human peritoneal mesothelial cells (HPMCs).
2018-10-18 | GSE121372 | GEO
Project description:Nonmuscle myosin IIB (NMIIB; heavy chain encoded by MYH10) is essential for cardiac myocyte cytokinesis. The role of NMIIB in other cardiac cells is not known. Here, we show that NMIIB is required in epicardial formation and functions to support myocardial proliferation and coronary vessel development. Ablation of NMIIB in epicardial cells results in disruption of epicardial integrity with a loss of E-cadherin at cell-cell junctions and a focal detachment of epicardial cells from the myocardium. NMIIB-knockout and blebbistatin-treated epicardial explants demonstrate impaired mesenchymal cell maturation during epicardial epithelial-mesenchymal transition. This is manifested by an impaired invasion of collagen gels by the epicardium-derived mesenchymal cells and the reorganization of the cytoskeletal structure. Although there is a marked decrease in the expression of mesenchymal genes, there is no change in Snail (also known as Snai1) or E-cadherin expression. Studies from epicardium-specific NMIIB-knockout mice confirm the importance of NMIIB for epicardial integrity and epicardial functions in promoting cardiac myocyte proliferation and coronary vessel formation during heart development. Our findings provide a novel mechanism linking epicardial formation and epicardial function to the activity of the cytoplasmic motor protein NMIIB.
2017-07-21 | GSE101701 | GEO
Project description:RNA-sequencing was carried out on ascetic fluid-isolated mesothelial cells from low-grade serous ovarian cancer patients, high-grade serous ovarian cancer patients, chemotherapy-treated high-grade serous ovarian cancer patients and control mesothelial cells obtained from non-oncologic patients to identify differentially expressed genes associated to mesothelial-to-mesenchymal transition process.
| EGAS00001003747 | EGA