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RNA-seq of injured mouse hearts depleted for myofibroblast Yap and Wwtr1

ABSTRACT: RNA-seq of injured mouse hearts depleted for myofibroblast Yap and Wwtr1

PROVIDER: PRJNA686945 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13280741.fastq.gz	Fastqsanger.gz
	SRR13280742.fastq.gz	Fastqsanger.gz
	SRR13280743.fastq.gz	Fastqsanger.gz
	SRR13280744.fastq.gz	Fastqsanger.gz
	SRR13280745.fastq.gz	Fastqsanger.gz

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RNA-seq of injured mouse hearts depleted for myofibroblast Yap and Wwtr1

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Assessing the effect of myofibroblast depletion for Yap and Wwtr1 by single Cell RNAsequencing within ventricular interstitial cells 6 days post surgical MI.

Project description:To assess the pathophysiological of genetic depletion of Yap and Wwtr1 in myofibroblasts following myocardial infarction, we utilized a Cre-lox system whereby the inducible Periostin promoter is leveraged to deplete both Yap and Wwtr1 from myofibroblasts in mice. Following myocardial infarction, myofibroblast depletion of both Yap and Wwtr1 significantly improves cardiac function after injury as compared to injured controls. Here, we have performed single cell RNA sequencing of interstitial cardiac cells 7 days post myocardial infarction to assess differentially express genes within cardiac fibroblasts and immune cell populations.

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RNA-seq of injured mouse hearts depleted for myofibroblast Yap or Yap and Wwtr1

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Multiple roles for Wwtr1 in cardiac wall maturation

Project description:Cardiac trabeculation is a highly regulated process that starts with the delamination of cardiomyocytes from the compact wall to form stereotypical muscular ridges in the developing ventricle. The Hippo signaling pathway has been implicated in cardiac development but many questions remain. We investigated the role of Wwtr1, a nuclear effector of the Hippo pathway, in zebrafish and find that its loss results in hearts with reduced trabeculation. However, in mosaic animals, wwtr1-/- cardiomyocytes contribute more frequently than wwtr1+/- cardiomyocytes to the trabecular layer of wild-type hearts. To investigate this paradox, we examined the myocardial wall at early stages and find that loss of Wwtr1 leads to disruption of the compact wall architecture, as evidenced by the disorganized cortical actin structure and abnormal cell-cell junctions. The mutant compact wall is not able to support trabeculation as, in mosaic animals, wild-type cardiomyocytes are more frequently in the compact layer of mutant than heterozygous hearts. Therefore, we propose that Wwtr1 establishes the compact wall architecture necessary for trabeculation and that it also modulates a cardiomyocyte’s decision to enter the trabecular layer.

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