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Age-Dependent Transcriptional Alterations in Cardiac Endothelial Cells

ABSTRACT: Age-Dependent Transcriptional Alterations in Cardiac Endothelial Cells

PROVIDER: PRJNA687680 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13302400.fastq.gz	Fastqsanger.gz
	SRR13302401.fastq.gz	Fastqsanger.gz
	SRR13302402.fastq.gz	Fastqsanger.gz
	SRR13302403.fastq.gz	Fastqsanger.gz
	SRR13302404.fastq.gz	Fastqsanger.gz

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Age-Dependent Transcriptional Alterations in Cardiac Endothelial Cells [scRNA-seq]

Project description:Age-Dependent Transcriptional Alterations in Cardiac Endothelial Cells [scRNA-seq]

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Age-Dependent Transcriptional Alterations in Cardiac Endothelial Cells [bulk RNA-seq]

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Age-Dependent Transcriptional Alterations in Cardiac Endothelial Cells [bulk RNA-seq]

Project description:Purpose: The goal of this study is to determine alterations in heart endothelial cell transcripts associated with aging. This is accomplished by comparing endothelial transcriptomes from young and aged organs (heart, brain and kidney). Methods: Endothelial mRNA profiles of 3 month and 24 month old wild-type mice were generated by next generation sequencing using libraries generated via SmartSeq V4 chemistry (Takara) and sequenced on an HiSeq 2500 (Illuina). Tophat2 with default parameters was used to align the sequenced reads against the mouse genome using the GRCm38. HTSeq python software with default parameters was used to quantify the transcripts of the aligned reads using the corresponding GRCm38 gene annotation model from Ensembl. Results: Highly enriched populations of endothelial cells (ECs) isolated from the heart, brain and kidney of young (3 months) and old (24 months) C57/BL6 mice were profiled for RNA expression via bulk RNA sequencing. Approximately 700 cardiac endothelial transcripts significantly differ by age. Gene set enrichment analysis indicated similar patterns for cellular pathway perturbations. Receptor-ligand comparisons indicated parallel alterations in age-affected circulating factors and cardiac endothelial-expressed receptors. Single-cell RNA-seq analysis identified 9 distinct endothelial cell subtypes in the heart with an age-associated population shift observed for an Aplnr-enriched endothelial cell clusters. Conclusions: Gene and pathway enrichment analyses show that age-related transcriptional response of cardiac endothelial cells is distinct from that of endothelial cells derived from the brain or kidney vascular bed. Furthermore, single-cell analysis identified 9 distinct EC subtypes, and shows that Aplnr-enriched subtype is reduced with age in mouse heart. Finally, we identify age-dysregulated genes in specific aged cardiac endothelial subtypes.

2021-05-28 | GSE163821 | GEO

Age-Dependent Transcriptional Alterations in Cardiac Endothelial Cells [scRNA-seq]

Project description:Purpose: The goal of this study is to determine alterations in heart endothelial cell transcripts and cell populations associated with aging. Methods: Endothelial single cell mRNA profiles of 3 month and 24 month old wild-type mice were generated by 10X Genomics Results: Using an optimized data analysis workflow, we mapped about 50 thousand reads per cell Conclusions: Our study represents the first analysis of aged cardiac endothelial cell transcriptomes using single cell RNA-seq technology, identifiying specific transcripts and cell populations affected by age.

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Age-dependent Lamin remodeling induces cardiac dysfunction via dysregulation of cardiac transcriptional programs

Project description:Age-dependent Lamin remodeling induces cardiac dysfunction via dysregulation of cardiac transcriptional programs

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Age-dependent transcriptional alterations in cardiac endothelial cells.

Project description:Aging is a significant risk factor for cardiovascular disease. Despite the fact that endothelial cells play critical roles in cardiovascular function and disease, the molecular impact of aging on this cell population in many organ systems remains unknown. In this study, we sought to determine age-associated transcriptional alterations in cardiac endothelial cells. Highly enriched populations of endothelial cells (ECs) isolated from the heart, brain, and kidney of young (3 mo) and aged (24 mo) C57/BL6 mice were profiled for RNA expression via bulk RNA sequencing. Approximately 700 cardiac endothelial transcripts significantly differ by age. Gene set enrichment analysis indicated similar patterns for cellular pathway perturbations. Receptor-ligand comparisons indicated parallel alterations in age-affected circulating factors and cardiac endothelial-expressed receptors. Gene and pathway enrichment analyses show that age-related transcriptional response of cardiac endothelial cells is distinct from that of endothelial cells derived from the brain or kidney vascular bed. Furthermore, single-cell analysis identified nine distinct EC subtypes and shows that the Apelin Receptor-enriched subtype is reduced with age in mouse heart. Finally, we identify age-dysregulated genes in specific aged cardiac endothelial subtypes.

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Age-dependent Lamin remodeling induces cardiac dysfunction via dysregulation of cardiac transcriptional programs [RNA-Seq]

Project description:As we age, structural changes contribute to progressive decline in organ function, which in the heart acts through poorly characterized mechanisms. Utilizing the rapidly aging fruit fly model with its significant homology to the human cardiac proteome, we found that cardiomyocytes exhibit progressive loss of Lamin C (mammalian Lamin A/C homologue) with age. Unlike other tissues and laminopathies, we observe decreasing nuclear size, while nuclear stiffness increases. Premature genetic reduction of Lamin C phenocopies aging’s effects on the nucleus, and subsequently decreases heart contractility and sarcomere organization. Surprisingly, Lamin C reduction downregulates myogenic transcription factors and cytoskeletal regulators, possibly via reduced chromatin accessibility. Subsequently, we find an adult-specific role for cardiac transcription factors and show that maintenance of Lamin C sustains their expression and prevents age-dependent cardiac decline. Our findings are conserved in aged non-human primates and mice, demonstrating age-dependent nuclear remodeling is a major mechanism contributing to cardiac dysfunction.

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Age-dependent Lamin remodeling induces cardiac dysfunction via dysregulation of cardiac transcriptional programs [ATAC-Seq]

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Age-dependent increase of oxidative stress regulates microRNA-29 family preserving cardiac health

Project description:The short-lived turquoise killifish Nothobranchius furzeri (Nfu) is a valid model for aging studies. Here, we investigated its age-associated cardiac function. We observed oxidative stress accumulation and an engagement of microRNAs (miRNAs) in the aging heart. MiRNA-sequencing of 5 week (young), 12-21 week (adult) and 28-40 week (old) Nfu hearts revealed 23 up-regulated and 18 down-regulated miRNAs with age. MiR-29 family turned out as one of the most up-regulated miRNAs during aging. MiR-29 family increase induces a decrease of known targets like collagens and DNA methyl transferases (DNMTs) paralleled by 5´methyl-cytosine (5mC) level decrease. To further investigate miR-29 family role in the fish heart we generated a transgenic zebrafish model where miR-29 was knocked-down. In this model we found significant morphological and functional cardiac alterations and an impairment of oxygen dependent pathways by transcriptome analysis leading to hypoxic marker up-regulation. To get insights the possible hypoxic regulation of miR-29 family, we exposed human cardiac fibroblasts to 1% O2 levels. In hypoxic condition we found miR-29 down-modulation responsible for the accumulation of collagens and 5mC. Overall, our data suggest that miR-29 family up-regulation might represent an endogenous mechanism aimed at ameliorating the age-dependent cardiac damage leading to hypertrophy and fibrosis.

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Age-dependent Lamin remodeling induces cardiac dysfunction via dysregulation of cardiac transcriptional programs [ATAC-Seq]

Project description:Age-dependent Lamin remodeling induces cardiac dysfunction via dysregulation of cardiac transcriptional programs [ATAC-Seq]

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