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Loss of ADAMTS19 causes progressive non-syndromic heart valve disease

ABSTRACT: Loss of ADAMTS19 causes progressive non-syndromic heart valve disease

PROVIDER: PRJNA430237 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6496010_1.fastq.gz	Fastqsanger.gz
	SRR6496010_2.fastq.gz	Fastqsanger.gz
	SRR6496020_1.fastq.gz	Fastqsanger.gz
	SRR6496020_2.fastq.gz	Fastqsanger.gz
	SRR6496011_1.fastq.gz	Fastqsanger.gz

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Loss of ADAMTS19 causes progressive non-syndromic heart valve disease

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Loss of ADAMTS19 causes progressive non-syndromic heart valve disease.

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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.

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Project description:Therapeutic management of heart valve disease is currently hampered by a lack of mechanistic understanding of human valve development and pathobiology. Here, we develop a protocol to generate 3-dimensional human heart valve tissues from pluripotent stem cells with enhanced maturational properties closely mirroring the valve interstitial cell, resident myeloid cells and protein expression profile of native heart valves. Importantly, bioengineered heart valves transplanted subcutaneously in rats did not calcify, highlighting potential clinical utility as a cellular therapy. In parallel, using a high-throughput 96-well platform, we demonstrate that bioengineered human heart valves can be used for modelling valve disease. Treatment with inflammatory cytokines augmented tissue passive tension and upregulated molecular markers associated with valve calcification and fibrosis. Thus, bioengineered human heart valve tissues provide a platform to understand human heart valve development, disease pathogenesis and offer a potential regenerative therapy for heart valve disease.

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