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RNA-Seq of injured mouse hearts depleted for myofibroblast Yap [I]

ABSTRACT: RNA-Seq of injured mouse hearts depleted for myofibroblast Yap [I]

PROVIDER: PRJNA685438 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13257537.fastq.gz	Fastqsanger.gz
	SRR13257538.fastq.gz	Fastqsanger.gz
	SRR13257539.fastq.gz	Fastqsanger.gz
	SRR13257540.fastq.gz	Fastqsanger.gz
	SRR13257541.fastq.gz	Fastqsanger.gz

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

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

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

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

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RNA-Seq of injured mouse hearts depleted for myofibroblast Yap [I]

Project description:A myofibroblast specific tamoxifen inducible Cre was used to assess the contribution of Yap in the mouse heart after myocardial infarction

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

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

Project description:This SuperSeries is composed of the SubSeries listed below.

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Myofibroblast YAP/TAZ activation is a key step in organ fibrogenesis

Project description:Fibrotic diseases account for nearly half of all deaths in the developed world. Despite its importance, the pathogenesis of fibrosis remains poorly understood. Recently, the two mechanosensitive transcription cofactors YAP and TAZ have emerged as important profibrotic regulators in multiple murine tissues. Despite this growing recognition, a number of important questions remain unanswered, including which cell types require YAP/TAZ activation for fibrosis to occur and the time course of this activation. Here, we present a detailed analysis of the role that myofibroblast YAP and TAZ play in organ fibrosis and the kinetics of their activation. Using analyses of cells, as well as multiple murine and human tissues, we demonstrated that myofibroblast YAP and TAZ were activated early after organ injury and that this activation was sustained. We further demonstrated the critical importance of myofibroblast YAP/TAZ in driving progressive scarring in the kidney, lung, and liver, using multiple transgenic models in which YAP and TAZ were either deleted or hyperactivated. Taken together, these data establish the importance of early injury-induced myofibroblast YAP and TAZ activation as a key event driving fibrosis in multiple organs. This information should help guide the development of new antifibrotic YAP/TAZ inhibition strategies.

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Characterization of myocardial B cells in naïve hearts, acutely injured hearts and acutely injured hearts of mice treated with Pirfenidone

Project description:Characterization of myocardial B cells in naïve hearts, acutely injured hearts and acutely injured hearts of mice treated with Pirfenidone

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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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2018-12-25 | GSE112984 | GEO

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