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

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

ORGANISM(S): Mus musculus

PROVIDER: GSE163269 | GEO | 2022/10/29

REPOSITORIES: GEO

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

Project description:A myofibroblast specific tamoxifen inducible Cre was used to assess the role of Yap and Wwtr1 in the mouse heart after myocardial infarction

2022-10-29 | GSE163612 | GEO

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.

2023-02-27 | GSE204712 | GEO

Genetic lineage tracing defines myofibroblast origin and function in the injured heart

Project description:Cardiac fibroblasts convert to myofibroblasts with injury to mediate healing after acute myocardial infarction and to mediate long-standing fibrosis with chronic disease. Myofibroblasts remain a poorly defined cell-type in terms of their origins and functional effects in vivo. Methods: Here we generate Postn (periostin) gene-targeted mice containing a tamoxifen inducible Cre for cellular lineage tracing analysis. This Postn allele identifies essentially all myofibroblasts within the heart and multiple other tissues. Results: Lineage tracing with 4 additional Cre-expressing mouse lines shows that periostin-expressing myofibroblasts in the heart derive from tissue-resident fibroblasts of the Tcf21 lineage, but not endothelial, immune/myeloid or smooth muscle cells. Deletion of periostin+ myofibroblasts reduces collagen production and scar formation after myocardial infarction. Periostin-traced myofibroblasts also revert back to a less activated state upon injury resolution. Conclusions: Our results define the myofibroblast as a periostin-expressing cell-type necessary for adaptive healing and fibrosis in the heart, which arises from Tcf21+ tissue-resident fibroblasts. Fluidigm C1 whole genome transcriptome analysis of lineage mapped cardiac myofibroblasts

2016-06-14 | E-GEOD-83337 | biostudies-arrayexpress

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

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

| PRJNA685438 | ENA

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

| PRJNA686940 | ENA

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

| PRJNA686945 | ENA

Genetic lineage tracing defines myofibroblast origin and function in the injured heart

2016-06-14 | GSE83337 | GEO

Cardiac-specific YAP activation improve cardiac function and survival in an experimental murine MI model

Project description:In this study, we used a cardiac-specific, inducible expression system to activate YAP in adult mouse heart. Activation of YAP in adult heart promoted cardiomyocyte proliferation and did not deleteriously affect heart function. Furthermore, YAP activation after myocardial infarction (MI) preserved heart function and reduced infarct size. Using adeno-associated virus subtype 9 (AAV9) as a delivery vector, we expressed human YAP in the murine myocardium immediately after MI. We found that AAV9:hYAP significantly improved cardiac function and mouse survival. AAV9:hYAP did not exert its salutary effects by reducing cardiomyocyte apoptosis. Rather, we found that AAV9:hYAP stimulated adult cardiomyocyte proliferation. Gene expression profiling indicated that AAV9:hYAP stimulated cell cycle gene expression, enhanced TGFβ-signaling, and activated of components of the inflammatory response.Cardiac specific YAP activation after MI mitigated myocardial injury after MI, improved cardiac function and mouse survival. These findings suggest that therapeutic activation of hYAP or its downstream targets, potentially through AAV-mediated gene therapy, may be a strategy to improve outcome after MI. Three groups were involved in this study: sham group, AAV9:Luci+MI group and AAV9-YAP+MI group. Each group contained three biological replicates. The sham group had neither myocardial infarction nor AAV injection. The AAV9:Luci +MI(L for brief) group had myocardial infarction and injected with AAV9:Luic. The AAV9:hYAP+MI(YAP for brief) group had myocardial infarction and injected with AAV9:hYAP. 5 days after MI and AAV injection, the heart apexes were collected and the total RNA were isolated for microarray analysis.

2014-05-26 | E-GEOD-54612 | biostudies-arrayexpress

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.

2022-10-29 | GSE163617 | GEO

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.

2022-02-22 | GSE135327 | GEO

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