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Foxa2 identifies a novel ventricular-specific cardiac progenitor population during gastrulation.

ABSTRACT: The recent identification of novel progenitor populations that contribute to the developing heart in a distinct temporal and spatial manner has fundamentally improved our understanding of cardiac development. However, little remains known about cardiac specification events prior to the establishment of the heart tube, or the mechanisms that direct atrial versus ventricular specification. We have identified a novel progenitor population that gives rise specifically to cardiovascular cells of the ventricles but not the atria, and to the epicardium of the differentiated heart. We determined that this cell population is first specified during gastrulation, when it transiently expresses Foxa2, a gene not previously implicated in cardiac development. Using chimeric mosaic analysis we further demonstrate that Foxa2 is cell-autonomously required for the development of ventricular cells. Finally, we reveal the existence of an analogous Foxa2+ cardiac mesoderm population during in vitro differentiation from embryonic stem cells and illustrate that these cells express genes relevant for heart development. Our data thus describe the first progenitor population identified as early as gastrulation that displays ventricular-specific differentiation potential. Together, these findings provide important new insights into the developmental origin of ventricular and atrial myocytes, and will lead to the establishment of new strategies for generating these cell types from pluripotent stem cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE78964 | GEO | 2017/02/08

SECONDARY ACCESSION(S): PRJNA314510

REPOSITORIES: GEO

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Mus musculus

Project description:Foxa2 identifies a novel ventricular-specific cardiac progenitor population during gastrulation.

| PRJNA314510 | ENA

Single Cell Transcriptomic Profiling of Cardiac Tissues and Surrounding Tissues During Early Cardiac Development

Project description:The specification of distinct cardiac lineages during development is thought to occur prior to the morphogenetic events that lead to chamber formation and acquisition of bona fide atrial or ventricular identity. However, the mechanisms underlying these dynamic early specification events remain poorly understood. In this study, we performed single cell analysis across the time window of progenitor specification, namely at the cardiac crescent (E8.25), primitive heart tube (E8.75) and heart tube (E9.25) stages to uncover the transcriptional heterogeneity of early progenitor cells ,as well as mechanisms underlying differentiation of atrial and ventricular cardiomyocytes and associated cardiac cell types.

2022-06-15 | GSE205950 | GEO

Macrophage Precursor Cells from the Left Atrial Appendage of the Adult Heart Spontaneously Reprogram into a C-kit+/CD45- Stem Cell-Like Phenotype [Array analysis]

Project description:The developmental origin of the c-kit expressing progenitor cell pool in the adult heart has remained elusive. Recently, it has been discovered that the injured heart is enriched with c-kit+ cells, which also express the hematopoietic marker CD45. In this study, we characterize the phenotype and transcriptome of the c-kit+/CD45+ cell population, originating from the left atrial appendage. These cells are defined as cardiac macrophage progenitors. We also demonstrate that the c-kit+/CD45+ progenitor cell population activates heart development, neural crest and pluripotency associated pathways in vitro, in conjunction with CD45 down-regulation, and acquire a c-kit+/lin- phenotype. This spontaneous reprogramming progresses further to a highly proliferative, partially myogenic phenotype. Our data suggests that c-kit+/lin- cells and cardiac macrophages have a common lineage origin possibly resolving some current conundrums in the field of cardiac regeneration. Two different stem cell types were grown by altering the tissue digestion protocol. To investigate their transcriptional profiles we prepared RNA from two cell sorted replicates per cell type and from two left ventricular biopsy samples as controls.

2016-07-03 | E-GEOD-57064 | biostudies-arrayexpress

Genetic profiling and surface proteome analysis of epicardial derived cells reveals cardiogenic potential

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

PRDM16 is required for proper specification of the working ventricular myocardium by suppressing alternative cardiomyocyte cell fates.

Project description:PRDM16 is a transcription factor with histone methyltransferase activity expressed at the earliest stages of cardiac development. Pathogenic mutations in humans lead to cardiomyopathy, conduction abnormalities and heart failure. PRDM16 is specifically expressed in ventricular but not atrial cardiomyocytes and declines in expression postnatally. Since in other tissues PRDM16 is best known for its role in binary cell fate decisions, we hypothesized a similar decision-making function in cardiomyocytes. Here, we demonstrated that cardiomyocyte-specific deletion of Prdm16 during cardiac development results in contractile dysfunction and abnormal electrophysiology of the postnatal heart, resulting in premature death. By combined RNA+ATAC single-cell sequencing we found that PRDM16 favors ventricular working cardiomyocyte identity, by opposing the activity of master regulators of atrial and ventricular conduction fate. Myocardial loss of Prdm16 during development resulted in hyperplasia of the ventricular conduction system. Hence, PRDM16 plays an indispensable role during cardiac development by driving ventricular working cardiomyocyte identity.

2024-09-18 | GSE255382 | GEO

RNA sequencing of murine ESC-derived cardiac progenitor cells treated with screening hit compound Cucurbitacin I Hydrate

Project description:Cucurbitacin I Hydrate promotes selection towards atrial cardiac fate when cardiac progenitor cells are treated with the compound. RNA sequencing was performed to assess transcript expression of signaling pathways or regulators of atrial or ventricular cardiac differentiation.

2023-03-17 | GSE128609 | GEO

Transcriptional changes associated with advancing stages of heart failure underlie atrial and ventricular arrhythmogenesis underlie atrial and ventricular arrhythmogenesis

Project description:Heart failure (HF) is a leading cause of mortality and is associated with cardiac remodeling. Vulnerability to atrial fibrillation (AF) has been shown to be greater in the early stages of HF, whereas ventricular tachycardia/fibrillation develop during late stages. Here, we explore changes in gene expression that underlie the differential development of fibrosis and structural alterations that predispose to atrial and ventricular arrhythmias.

2019-01-01 | GSE123823 | GEO

Transcription profiling of normal atria and ventricles

Project description:Pharmacological and gene ablation studies have demonstrated a crucial role of the cardiac natriuretic peptides (NP) hormones ANF and BNP in the maintenance of cardiovascular homeostasis. In addition, hypertension and chronic congestive heart failure are clinical entities that may be regarded as states of relative NP deficiency. Hence the study of the function of the endocrine heart is highly relevant. To identify genes that are related to the endocrine function of the heart we have conducted differential gene expression studies of the rat atria and ventricles using oligonucleotide arrays. Experiment Overall Design: The atrial appendages and the ventricular free walls were obtained from thirteen normal male Sprague Dawley rats. The total RNA was obtained from four pools of atrial and four pools of ventricular tissues. Four biological replicates for each muscle type were generated, i.e. 4 atrial replicates and 4 ventricular replicates.

2009-09-15 | E-GEOD-5266 | biostudies-arrayexpress

Macrophage Precursor Cells from the Left Atrial Appendage of the Adult Heart Spontaneously Reprogram into a C-kit+/CD45- Stem Cell-Like Phenotype [RNA-Seq]

Project description:The developmental origin of the c-kit expressing progenitor cell pool in the adult heart has remained elusive. Recently, it has been discovered that the injured heart is enriched with c-kit+ cells, which also express the hematopoietic marker CD45. In this study, we characterize the phenotype and transcriptome of the c-kit+/CD45+ cell population, originating from the left atrial appendage. These cells are defined as cardiac macrophage progenitors. We also demonstrate that the c-kit+/CD45+ progenitor cell population activates heart development, neural crest and pluripotency associated pathways in vitro, in conjunction with CD45 down-regulation, and acquire a c-kit+/lin- phenotype. This spontaneous reprogramming progresses further to a highly proliferative, partially myogenic phenotype. Our data suggests that c-kit+/lin- cells and cardiac macrophages have a common lineage origin possibly resolving some current conundrums in the field of cardiac regeneration. Two different stem cell types were grown by altering the tissue digestion protocol, from which one type was spontaneously transdifferentiating to other cell types. To investigate their transcriptional profiles we prepared RNA from two cell sorted replicates per cell type (A, B, C1, C2, C3).

2016-07-03 | E-GEOD-57125 | biostudies-arrayexpress

Molecular Remodeling of Ion Channels in Human Atrial and Ventricular Myocytes Associated with Ischemic Cardiomyopathy

Project description:Ischemic cardiomyopathy (ICM) leads to congestive heart failure and can cause sudden cardiac death due to arrhythmia. Existing molecular knowledge base of ICM is rudimentary because of lack of specific attribution to cell type and function. This study was designed to investigate cell-specific molecular remodeling of ion channels, exchangers and pumps, which are signaling molecules (SM) involved in electrical, signaling and mechanical functions of the heart. Atrial and ventricular myocytes were isolated by laser-capture microdissection from left atrium and ventricle of healthy and ICM human hearts. SM and their splice variants altered by ICM in cardiomyocytes were identified by splice microarray and validated by RT-PCR. Molecular profiling of ICM-related changes showed that SM in atrial and ventricular myocytes remodel following their unique programs. ICM affected 63 genes in ventricular myocytes and 12 genes in atrial myocytes. Only few of the identified genes were previously linked to human cardiac disfunctions. In our experiments we used 3 healthy hearts rejected from transplantation procedure and explanted ICM hearts from three male patients. Tissue samples were dissected from left ventricle and left atrial appendages. Atrial and ventricular myocytes were laser-capture microdissected from serial 7-8-Âµm thick cryostat sections. Individual cellular total RNA samples were analyzed on custom-built Human Ion Channel Splice Arrays slides (ExonHit) manufactured on the Ion Channel Splice Array sv1.1 platform representing 287 human SM, including 248 alternatively spliced ones in total 1655 splicing events and supplemented with capabilities to recognize connexins and ryanodine receptors.

2010-05-14 | E-GEOD-17294 | biostudies-arrayexpress

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