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RNA-Seq of rat cardiac fibroblasts depleted for Yap and Wwtr1

ABSTRACT: RNA-Seq of rat cardiac fibroblasts depleted for Yap and Wwtr1

PROVIDER: PRJNA768827 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16206850.fastq.gz	Fastqsanger.gz
	SRR16206851.fastq.gz	Fastqsanger.gz
	SRR16206852.fastq.gz	Fastqsanger.gz
	SRR16206853.fastq.gz	Fastqsanger.gz
	SRR16206854.fastq.gz	Fastqsanger.gz

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RNA-Seq of rat cardiac fibroblasts depleted for 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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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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Human Cardiac Fibroblast BioID2 Interactome for SKI and TAZ(WWTR1)

Project description:We used adenoviral-mediated overexpression of MYC-BioID2, MYC-BioID2-SKI, MYC-BioID2-WWTR1 (TAZ) in human primary cardiac fibroblasts to elucidate the interaction between SKI and the Hippo signaling pathway. Original data is also available on the Global Proteome Machine (http://hs2.proteome.ca/tandem/thegpm_tandem.html). Datasets are identified as follows: GPM10000002938 and 2939 are untreated negative control cell lysates; GPM10000002941 and 2942 are "empty" MYC-BioID2 vector; GPM10000002943 and 2944 are MYC-BioID2-SKI; and GPM10000002944 and 2945 are MYC-BioID2-WWTR1(TAZ).

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ErbB2 drives Yap activation during cardiac regeneration

Project description:Cardiomyocyte (CM) loss after injury results in adverse remodelling and fibrosis, which inevitably lead to heart failure. Neuregulin-ErbB2 and Hippo-Yap signaling pathways are key mediators of CM proliferation and regeneration although the crosstalk between these pathways is unclear. Here, we demonstrate in mice that temporal over-expression (OE) of activated ErbB2 in CMs promotes cardiac regeneration in a heart failure model. Cellularly, OE CMs present an EMT-like regenerative response involving cytoskeletal reprograming, migration, ECM turnover, and displacement. Molecularly, we identified Yap as a critical mediator of ErbB2 signaling. In OE CMs, Yap interacts with nuclear envelope and cytoskeletal components, reflective of the altered mechanic state elicited by ErbB2. Hippo-independent activating phosphorylation on Yap at S352 and S274 were enriched in OE CMs, peaking during metaphase. Viral overexpression of Yap phospho-mutants dampened the proliferative competence of OE CMs. Taken together, we demonstrate a potent ErbB2-mediated Yap mechanosensory signaling involving EMT-like characteristics, resulting in heart regeneration.

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