Danio rerio
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ABSTRACT:
PROVIDER: PRJNA371293 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Atrial Molecular Asymmetry Precedes the Emergence of Cardiac Septation I
| PRJNA371294 | ENA
Project description:Atrial Molecular Asymmetry Precedes the Emergence of Cardiac Septation
| PRJNA369836 | ENA
Project description:Atrial Molecular Asymmetry Precedes the Emergence of Cardiac Septation [RNA-seq]
| PRJNA413070 | ENA
Project description:Co-development of the lungs and heart underlies key evolutionary innovations in the transition to terrestrial life. Cardiac specializations that support pulmonary circulation, including the atrial septum, are generated by second heart field (SHF) cardiopulmonary progenitors (CPPs). It has been presumed that transcription factors required in the SHF for cardiac septation, e.g. Tbx5, directly drive a cardiac morphogenesis gene regulatory network. Here, we report instead that TBX5 directly drove Wnt ligands to initiate a bi-directional signaling loop between cardiopulmonary mesoderm and the foregut endoderm for endodermal pulmonary specification, and subsequently, atrial septation. TBX5 ChIP-seq identified cis-regulatory elements at Wnt2 sufficient for endogenous Wnt2 expression domains in vivo and required for Wnt2 expression in pre-cardiac mesoderm in vitro. Thus, Tbx5 initiated a mesoderm-endoderm-mesoderm signaling loop in lunged vertebrates that provides a molecular basis for the co-evolution of pulmonary and cardiac structures required for terrestrial life.
2018-10-22 | GSE119885 | GEO
Project description:Integrated cell-to-cell signaling networks regulate vertebrate axis formation and left-right asymmetry
| PRJNA119961 | ENA
Project description:The Pitx2 gene encodes a homeobox transcription factor that is required for mammalian development. Disruption of PITX2 expression in humans causes congenital heart diseases and is associated with atrial fibrillation (AF), however, the cellular and molecular processes dictated by Pitx2 during cardiac ontogeny remain unclear. To characterize the role of Pitx2 during murine heart development we sequenced over 75,000 single cardiac cell transcriptomes between two key developmental timepoints in control and Pitx2-null embryos. We uncovered that cardiac cell composition was dramatically altered in mutants at both E10.5 and E13.5. Interestingly, the differentiation dynamics of both anterior and posterior second heart field derived progenitor cells were disrupted in Pitx2 mutants. We also uncovered evidence for defects in left-right asymmetry within atrial cardiomyocyte populations. Furthermore, we were able to detail defects in cardiac outflow tract and valve development associated with Pitx2. Our findings offer insight into Pitx2 biology and provide a compilation of gene expression signatures for further detailing the complexities of heart development that will serve as the foundation for future studies of cardiac morphogenesis, congenital heart disease, and arrhythmogenesis.
2019-06-03 | GSE131181 | GEO
Project description:Objectives: We studied the signal transduction of atrial structural remodelling that contributes to the pathogenesis of atrial fibrillation (AF). Backround: Fibrosis is a hallmark of arrhythmogenic structural remodelling but the underlying molecular mechanisms are incompletely understood. Methods: We performed transcriptional profiling of left atrial myocardium (LA) from patients with AF and sinus rhythm (SR) and applied cultured primary cardiac cells and transgenic mice with overexpression of constitutively active V12Rac1 (RacET) who develop AF at old age to characterize mediators of the signal transduction of atrial remodeling. Results: LA from patients with AF showed a marked upregulation of connective tissue growth factor (CTGF) expression compared SR patients. This was associated with increased fibrosis, NADPH-oxidase-, Rac1- and RhoA activity, upregulation of N-cadherin and connexin 43 (Cx43) expression and increased angiotensin II tissue concentration. In neonatal rat cardiac myocytes and -fibroblasts, a specific small molecule inhibitor of Rac1 or simvastatin completely prevented the angiotensin II induced upregulation of CTGF, Cx43 and N-cadherin expression. Transfection with small-inhibiting CTGF RNA blocked Cx43 and N-cadherin expression. RacET mice showed upregulation of CTGF, Cx43 and N-cadherin protein expression. Inhibition of Rac1 by oral statin treatment prevented these effects, identifying Rac1 as a key regulator of CTGF in vivo. Conclusion: The data identify CTGF as an important mediator of atrial structural remodelling during AF. Angiotensin II activates CTGF via activation of Rac1 and NADPH oxidase, leading to upregulation of Cx43, N-cadherin and interstitial fibrosis and therefore contributing to the signal transduction of atrial structural remodelling. Array design study consists of 5 Atrial Fibrillation patients and matched 5 samples of patients in sinus rhythm (controls).
2010-02-21 | E-GEOD-14975 | biostudies-arrayexpress
Project description:Characterizing the cardiac neural crest in Danio rerio
| PRJNA1185249 | ENA