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Multi-chamber cardioids unravel human heart development and cardiac defects [RNA-Seq]

ABSTRACT: Multi-chamber cardioids unravel human heart development and cardiac defects [RNA-Seq]

PROVIDER: PRJNA862100 | ENA |

REPOSITORIES: ENA

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Multi-chamber cardioids unravel human heart development and cardiac defects

Project description:Multi-chamber cardioids unravel human heart development and cardiac defects

| PRJNA1001344 | ENA

Multi-chamber cardioids unravel human heart development and cardiac defects [scRNA-seq]

Project description:Multi-chamber cardioids unravel human heart development and cardiac defects [scRNA-seq]

| PRJNA1001348 | ENA

Multi-chamber cardioids unravel human heart development and cardiac defects [scRNA-seq]

Project description:The number one cause of human fetal death are defects in heart development. Because the human embryonic heart is inaccessible, and the impacts of mutations, drugs, and environmental factors on the specialized functions of different heart compartments are not captured by in vitro models, determining the underlying causes is difficult. Here, we established a human cardioid platform that recapitulates the development of all major embryonic heart compartments, including right and left ventricles, atria, outflow tract, and atrioventricular canal. By leveraging both 2D and 3D differentiation, we efficiently generated progenitor subsets with distinct first, anterior, and posterior second heart field identities. This advance enabled the reproducible generation of cardioids with compartment-specific in vivo-like gene expression profiles, morphologies, and functions. We used this platform to unravel the ontogeny of signal and contraction propagation between interacting heart chambers and dissect how genetic and environmental factors cause region-specific defects in the developing human heart.

2023-10-30 | GSE239890 | GEO

Multi-chamber cardioids unravel human heart development and cardiac defects [RNA-Seq]

2023-10-30 | GSE209677 | GEO

Multi-chamber cardioids unravel human heart development and cardiac defects

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-10-30 | GSE239891 | GEO

Molecular Signatures of cardiac defects in Down syndrome lymphoblastoid cell lines (congenital heart disease)

Project description:Molecular Signatures of cardiac defects in Down syndrome lymphoblastoid cell lines. In this study, we want to identify genes and pathways specifically dysregulated in atrioventricular septal defect and /or atrial septal defect + ventricular septal defect in case of trisomy 21. Total RNA obtained from DS lymphoblastoid cell lines without congenital heart disease compared to cell lines from DS with congenital heart disease.

2012-08-14 | E-GEOD-34457 | biostudies-arrayexpress

Molecular Signatures of cardiac defects in Down syndrome lymphoblastoid cell lines

Project description:This SuperSeries is composed of the following subset Series: GSE34457: Molecular Signatures of cardiac defects in Down syndrome lymphoblastoid cell lines (congenital heart disease) GSE34458: Molecular Signatures of cardiac defects in Down syndrome lymphoblastoid cell lines (trisomy 21) Refer to individual Series

2012-08-14 | E-GEOD-34459 | biostudies-arrayexpress

Myocardial Bmp2 overexpression leads to ectopic cardiac EMT and promotes chamber cardiomyocyte proliferation and immaturity

Project description:Defective valve and septa formation constitute a substantial part of congenital heart defects affecting the neonate or the adult. During cardiac development, restricted myocardial Bmp2 expression is a key signal for the specification and patterning of the valve-forming field in the atrio-ventricular canal (AVC) region and the initiation of the epithelial-mesenchyme transition (EMT) that gives rise to the valve primordia. We have generated a mouse transgenic line conditionally expressing Bmp2. Nkx2.5Cre-driven Bmp2 overexpression in the myocardium leads to foetal lethality, due to valve and chamber dysmorphogenesis, and rescue of the AVC specification defect of Bmp2-null embryos. Nkx2.5Cre/+;Bmp2tg/+ transgenic embryos show ventricular septal defect, thickened valves, enlarged trabeculae and dilated ventricles, whose endocardium is able to undergo EMT when explanted onto collagen gels. Gene profile and marker analysis indicates that cellular proliferation is increased and chamber differentiation and patterning is impaired in Nkx2.5Cre/+;Bmp2tg/+ embryos, but the ventricular-specific gene expression program is not abolished. We obtained similar results using a second myocardial driver (cTnTCre) to activate Bmp2 expression, but not with an endothelial-specific one (Tie2Cre), as Tie2Cre/+;Bmp2tg/+ mice are normal and survive to adulthood, indicating that Bmp2 must emanate from the myocardium to exert its EMT-driving and cardiomyocyte maturation blocking effect. Forced Bmp2 expression in vitro stimulates EBs proliferation and blocks their progression into cardiomyogenesis, an effect partially rescued by Noggin. These data show that widespread myocardial Bmp2 expression directs ectopic valve primordium formation and maintains chamber myocardium and early cardiac progenitors in a primitive, proliferative state, identifying Bmp2 as a potential factor for the expansion of immature cardiomyocytes.

2018-04-11 | GSE100810 | GEO

Molecular Signatures of cardiac defects in Down syndrome lymphoblastoid cell lines (congenital heart disease)

2012-08-15 | GSE34457 | GEO

USP28 Serves as A Key Suppressor of Mitochondrial Morphofunctional Defects and Cardiac Dysfunction in the Diabetic Heart [RNA-seq]

Project description:The majority of diabetics are susceptible to cardiac dysfunction and heart failure, while conventional drug therapy cannot correct diabetic cardiomyopathy (DCM) progression. Herein, we assessed the potential role and therapeutic value of ubiquitin-specific protease 28 (USP28) on the metabolic vulnerability of DCM. cardiac USP28 deficient diabetic mice showed cardiac dysfunction, lipid accumulation, and mitochondrial disarrangement, compared to their controls. Conversely, USP28 overexpression improved systolic and diastolic dysfunction and ameliorated cardiac hypertrophy and fibrosis in the diabetic heart. Mechanistically, USP28 directly interacted with peroxisome proliferator-activated receptor α (PPARα), deubiquitinating and stabilizing PPARα (Lys152) to promote mitofusin 2 (Mfn2) transcription, thereby impeding mitochondrial morphofunctional defects.

2023-10-15 | GSE244904 | GEO

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