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Identification of TGF-b targets in the cardiac outflow tract by transcriptomic analysis

ABSTRACT: Identification of TGF-b targets in the cardiac outflow tract by transcriptomic analysis

PROVIDER: PRJNA601645 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10902600.fastq.gz	Fastqsanger.gz
	SRR10902601.fastq.gz	Fastqsanger.gz
	SRR10902598.fastq.gz	Fastqsanger.gz
	SRR10902599.fastq.gz	Fastqsanger.gz

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Identification of TGF-b targets in the cardiac outflow tract by transcriptomic analysis

Project description:Purpose: identifying, with RNA-seq, genes targets of Alk5 during the development of the cardiac outflow tract in zebrafish. Results: we identified several differential expressed genes, with an enrichment in ECM component genes. As a proof of concept, many TGFb known targets also appeared downregulated.

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Expression data from the neural crest cells isolated from mouse cardiac outflow tract at E10.5

Project description:Neural crest defects lead to congenital heart disease involving outflow tract (OFT) malformation. Integrin-linked-Kinase (ILK) plays important roles in multiple cellular processes and embryogenesis. ILK is expressed in neural crest cells (NCC), but its role in NCC and OFT morphogenesis remains unknown. We used microarrays to detail the global programme of gene expression underlying the morphogenesis of the cardiac neural crest and outflow tract. The outflow tract of control and ILK mutant mouse embryos at E10.5 were dissected and dissociated. Neural crest cells were FACS sorted and used for RNA extraction and hybridization on Affymetrix microarrays.

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Expression data from the neural crest cells isolated from mouse cardiac outflow tract at E10.5

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An Anterior Second Heart Field Enhancer Regulates the Gene Regulatory Network of the Cardiac Outflow Tract

Project description:To identify a functional gene regulatory network that orchestrate transcriptional programs to direct proper outflow tract development, we generated transgenic mice harboring a 226bp-deletion within a GATA-dependent, highly conserved cardiac enhancer region. We then performed gene expression profiling analysis using data obtained from RNA-seq of outflow tract in wildtype and homozygous mutant littermates at embryonic day 12.5.

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Latent TGF β binding proteins 1 and 3 protect the larval zebrafish outflow tract from aneurysmal dilatation

Project description:Aneurysm and dissection of the aortic root is a common cause of morbidity and mortality in Loeys-Dietz Syndrome (LDS) and Marfan Syndrome (MFS), where perturbations in TGF β signaling play a causal or contributory role, respectively. Despite the advantages of cross-species disease modeling for mechanistic studies and pre-clinical drug discovery, animal models of aortic root aneurysm are largely restricted to genetically engineered mice. Here, we report that zebrafish larvae, homozygous for null mutations in latent TGF β binding proteins (ltbps) 1 and 3, develop rapid and severe aneurysmal dilatation of the aortic root equivalent, the outflow tract (OFT), after grossly unperturbed cardiac morphogenesis. The ventricle also becomes significantly dilated and upregulates stress-responsive genes, which likely reflects compensatory pathologic remodeling since ltbp1 and ltbp3 co-expression is restricted to the OFT. Similar to aneurysm tissue from LDS and MFS patients, the distended OFTs display evidence for hyperactivated TGF β signaling. Moreover, RNA-sequencing revealed significant overlap between the molecular signatures of diseased tissue from double knockout zebrafish and MFS mice. Lastly, chemical inhibition of the TGF β Type I receptor in wild-type embryos evoked similar OFT and ventricular dilation phenotypes, demonstrating that TGF β signaling is protective against these pathologies. The disease relevance of the mutant phenotype is further supported by recent family studies implicating genetic lesions in Ltbp3, and likely Ltbp1, as heritable causes of aortic root aneurysm. Ultimately, our data demonstrate that the unique advantages of zebrafish can now be leveraged to interrogate thoracic aneurysmal disease and identify novel lead compounds through small molecule suppressor screens.

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Cardiac Outflow tract septation defects in a DiGeorge syndrome model respond to Minoxidil treatment

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