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Unknown,Transcriptomics,Genomics,Proteomics

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Single cell sequencing of developing heart valves identifies novel cell populations and uncovers interstitial cell heterogeneity

ABSTRACT: This study has two main goals. The first is to define a gene expression atlas of heart valve cells and identify cell heterogeneity within postnatal heart valve development. The second is to identify interstitial cell populations involved in ECM remodeling during postnatal heart valve development. Overall design: Using droplet RNA sequencing, transcriptomes of single cells from P7 and P30 murine aortic and mitral heart valves were analyzed.

INSTRUMENT(S): Illumina HiSeq 2500

ORGANISM(S): Mus musculus

SUBMITTER: Alexia Hulin

PROVIDER: E-HCAD-18 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Maturation of heart valve cell populations during postnatal remodeling.

Hulin Alexia A Hortells Luis L Gomez-Stallons M Victoria MV O'Donnell Anna A Chetal Kashish K Adam Mike M Lancellotti Patrizio P Oury Cecile C Potter S Steven SS Salomonis Nathan N Yutzey Katherine E KE

Development (Cambridge, England) 20190312 12

Heart valve cells mediate extracellular matrix (ECM) remodeling during postnatal valve leaflet stratification, but phenotypic and transcriptional diversity of valve cells in development is largely unknown. Single cell analysis of mouse heart valve cells was used to evaluate cell heterogeneity during postnatal ECM remodeling and leaflet morphogenesis. The transcriptomic analysis of single cells from postnatal day (P)7 and P30 murine aortic (AoV) and mitral (MV) heart valves uncovered distinct sub ...[more]

PMID: 30796046

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Single cell sequencing of developing heart valves identifies novel cell populations and uncovers interstitial cell heterogeneity

Project description:Our study has two main goals. The first is to define a gene expression atlas of heart valve cells and identify cell heterogeneity within postnatal heart valve development. The second is to identify interstitial cell populations involved in ECM remodeling during postnatal heart valve development.

2018-07-13 | GSE117011 | GEO

ChIP-seq for Hoxa2 on mouse posterior branchial arches at E11.5

Project description:Hoxa2 ChIP-seq on mouse posterior branchial arches connected to outflow tract of the heart (PBA/OFT) at embryonic day (E) 11.5.

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ChIP-seq for Hoxa3 on mouse posterior branchial arches at E11.5.

Project description:Hoxa3 ChIP-seq on mouse posterior branchial arches connected to outflow tract of the heart (PBA/OFT) at embryonic day (E) 11.5.

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2020-10-16 | E-MTAB-8608 | biostudies-arrayexpress

Exploring the expression pattern of circRNA in the aortic valve

Project description:Calcific Aortic Valve Disease (CAVD) is a common heart valve condition, often characterized by severe narrowing of the aortic valve. It lacks pharmaceutical treatments and typically requires aortic valve replacement surgery, imposing a significant burden on healthcare resources.This study reports the expression profile of circRNAs in the aortic valve tissues of CAVD patients and a normal control group (non-CAVD). We collected aortic valve tissue samples from three CAVD patients who underwent aortic valve replacement surgery due to severe aortic valve stenosis, as well as aortic valve samples from non-CAVD patients who either received heart transplant surgery (recipient heart) or had their aortic valve removed due to aortic dissection. Overall, our research reveals the significant role of circRNAs in the progression of CAVD. CircRNAs, a class of circular non-coding RNA molecules, are actively studied for their functions and regulatory mechanisms within cells. These findings contribute to a deeper understanding of the molecular mechanisms underlying CAVD, particularly the potential involvement of circRNAs in this disease.

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SOX9 modulates the expression of key transcription factors required for heart valve development

Project description:Heart valve formation initiates when endothelial cells of the heart transform into mesenchyme and populate the cardiac cushions. The transcription factor, SOX9, is highly expressed in the cardiac cushion mesenchyme, and is essential for heart valve development. Loss of Sox9 in mouse cardiac cushion mesenchyme alters cell proliferation, embryonic survival, and disrupts valve formation. Despite this important role, little is known regarding how SOX9 regulates heart valve formation or its transcriptional targets. Therefore, we mapped putative SOX9 binding sites by ChIP-Seq in embryonic day (E) 12.5 heart valves, a stage at which the valve mesenchyme is actively proliferating and initiating differentiation. Embryonic heart valves have been shown to express a high number of genes that are associated with chondrogenesis, including several extracellular matrix proteins and transcription factors that regulate chondrogenesis. Consequently, we compared regions of putative SOX9 DNA-binding between E12.5 heart valves and E12.5 limb buds. We identified context-dependent and contextâindependent SOX9 interacting regions throughout the genome. Analysis of context-independent SOX9 binding suggests an extensive role for SOX9 across tissues in regulating proliferation-associated genes including key components of the AP-1 complex. Integrative analysis of tissue-specific SOX9 interacting regions and gene expression profiles on Sox9-deficient heart valves demonstrated that SOX9 controls the expression of several transcription factors with previously identified roles in heart valve development, including Twist1, Sox4, Mecom/Evi1 and Pitx2. Together, our data identifies SOX9 coordinated transcriptional hierarchies that control cell proliferation and differentiation during valve formation. Examination of SOX9 binding sites in E12.5 atrioventricular canal (AVC) and E12.5 embryonic limb and mRNA expression profiling in E12.5 WT and Sox9 mutant AVCs, in duplicate.

2015-11-05 | E-GEOD-73225 | biostudies-arrayexpress

SOX9 modulates the expression of key transcription factors required for heart valve development

Project description:Heart valve formation initiates when endothelial cells of the heart transform into mesenchyme and populate the cardiac cushions. The transcription factor, SOX9, is highly expressed in the cardiac cushion mesenchyme, and is essential for heart valve development. Loss of Sox9 in mouse cardiac cushion mesenchyme alters cell proliferation, embryonic survival, and disrupts valve formation. Despite this important role, little is known regarding how SOX9 regulates heart valve formation or its transcriptional targets. Therefore, we mapped putative SOX9 binding sites by ChIP-Seq in embryonic day (E) 12.5 heart valves, a stage at which the valve mesenchyme is actively proliferating and initiating differentiation. Embryonic heart valves have been shown to express a high number of genes that are associated with chondrogenesis, including several extracellular matrix proteins and transcription factors that regulate chondrogenesis. Consequently, we compared regions of putative SOX9 DNA-binding between E12.5 heart valves and E12.5 limb buds. We identified context-dependent and context–independent SOX9 interacting regions throughout the genome. Analysis of context-independent SOX9 binding suggests an extensive role for SOX9 across tissues in regulating proliferation-associated genes including key components of the AP-1 complex. Integrative analysis of tissue-specific SOX9 interacting regions and gene expression profiles on Sox9-deficient heart valves demonstrated that SOX9 controls the expression of several transcription factors with previously identified roles in heart valve development, including Twist1, Sox4, Mecom/Evi1 and Pitx2. Together, our data identifies SOX9 coordinated transcriptional hierarchies that control cell proliferation and differentiation during valve formation.

2015-11-05 | GSE73225 | GEO

Transcriptional Profiles of Aortic Valve from Calcific Aortic Valve Disease and Normal Control.

Project description:We report transcriptional profiles of aortic valve tissue from calcific aortic valve disease (CAVD) and normal control (non-CAVD). We collected the aortic valve tissues from five patients with CAVD who underwent aortic valve replacement due to severe aortic valve stenosis. Aortic valve samples from patients with non-calcified aortic valve resection due to heart transplantation (recipient heart) or aortic dissection were collected as the control (non-CAVD). The inclusion criteria for CAVD group were as follows: 50-75 years old; undergoing aortic valve replacement due to severe AVS with significantly valvular calcification. The inclusion criteria for non-CAVD group were as follows: non-calcified aortic valve resection due to heart transplantation (recipient heart) or aortic dissection. For each sample, total RNA was extracted, a cDNA library was generated, and an Illumina NovaSeq 6000 was used to sequence each sample. Stringtie software was used to count the fragment within each gene, and TMM algorithm was used for normalization. Differential expression analysis was performed using R package edgeR. Differentially expressed RNAs with |log2(FC)| value >1, q value [false discovery rate (FDR) adjusted P-value] <0.05, and one group’s mean fragments per kilobase of exon per million reads mapped (FPKM) >1, were assigned as differentially-expressed genes (DEGs).

2023-06-28 | GSE235995 | GEO

Understanding the cell fate and behavior of progenitors at the origin of the mouse cardiac mitral valve

Project description:Congenital heart malformations include mitral valve defects, which remain largely unexplained. During embryogenesis, a restricted population of endocardial cells within the atrioventricular canal undergoes an endothelial-to-mesenchymal transition to give rise to mitral valvular cells. However, the identity and fate decisions of these progenitors as well as the behavior and distribution of their derivatives in valve leaflets remain unknown. We used single-cell RNA sequencing (scRNA-seq) of genetically labeled endocardial cells and microdissected mouse embryonic and postnatal mitral valves to characterize the developmental road. We defined the metabolic processes underlying the specification of the progenitors and their contributions to subtypes of valvular cells. Using retrospective multicolor clonal analysis, we describe specific modes of growth and behavior of endocardial cell-derived clones, which build up, in a proper manner, functional valve leaflets. Our data identify how both genetic and metabolic mechanisms specifically drive the fate of a subset of endocardial cells toward their distinct clonal contribution to the formation of the valve.

2023-12-02 | GSE230849 | GEO

Single-cell analysis of T-cells from mouse neonate thymuses in a wild type control and a placental specific isoform of Igf2 knock-down (igf2-P0)

Project description:Fetal growth restriction (FGR) causes a wide variety of developmental defects in the neonate which can lead to heart disease, diabetes, anxiety and other disorders later in life. The effect of FGR on the immune system, however, is poorly understood. Immune cells throughout development are identified using cell-surface markers to distinguish between subtly different stages. These (surface) proteins, however, do not necessarily generate differences in cellular activity and may thus be only a coincidental shallow guide to classifying cells. High-throughput single-cell transcriptomics using DropSeq was performed on mouse neonate thymuses. The T-cell population was selected through flow cytometry in wild type controls and a placental specific isoform of Igf2 knock-down (igf2-p0). Using this analysis, we discovered skewed T-cell populations in the growth restricted murine neonate indicating a developmental delay. This finding recapitulates the altered immunity found in growth restricted human infants. The T-cell deficit persisted into adulthood, even when body and organ weights approached normal levels due to catch-up growth. This reduction in T-cellularity may have significant implications in adult immunity, adding to the wide variety of fetal origins for adult disease already known.

2018-11-06 | E-MTAB-6945 | biostudies-arrayexpress

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