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Wnt5a-YAP signaling axis mediates mechanotransduction in cardiac myocytes and contributes to the transition to heart failure

ABSTRACT: Wnt5a-YAP signaling axis mediates mechanotransduction in cardiac myocytes and contributes to the transition to heart failure

PROVIDER: PRJNA825762 | ENA |

REPOSITORIES: ENA

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Wnt5a-YAP signaling axis mediates mechanotransduction in cardiac myocytes and contributes to the transition to heart failure (rat sample)

Project description:Non-canonical Wnt signaling activated by Wnt5a and Wnt11 is required for the development of second heart field cardiac progenitor cells in mice. However, the pathophysiological role of non-canonical Wnt signaling in the adult heart has not been fully elucidated. Here we show that cardiomyocyte-specific Wnt5a knockout mice exhibit improved systolic function and reduced expression of mechanosensitive genes including Nppb compared to control mice when subjected to pressure overload. In cultured cardiac myocytes, Wnt5a knockdown reduces the upregulation of Nppb gene expression and YAP nuclear translocation induced by cyclic cell stretch. Wnt5a knockdown-induced Nppb downregulation in response to cell stretch is rescued by inhibition of Hippo pathway, and the rescue effect of Hippo inhibition is canceled by YAP knockdown. These results collectively suggest that Wnt5a-YAP signaling axis mediates mechanotransduction in cardiac myocytes and contributes to the transition to heart failure.

2023-07-17 | GSE200666 | GEO

Wnt5a-YAP signaling axis mediates mechanotransduction in cardiac myocytes and contributes to the transition to heart failure (mouse sample)

2023-07-17 | GSE200665 | GEO

Wnt5a-YAP signaling axis mediates mechanotransduction in cardiac myocytes and contributes to the transition to heart failure (mouse sample)

Project description:Wnt5a-YAP signaling axis mediates mechanotransduction in cardiac myocytes and contributes to the transition to heart failure (mouse sample)

| PRJNA825769 | ENA

Wnt5a-YAP signaling axis mediates mechanotransduction in cardiac myocytes and contributes to the transition to heart failure (rat sample)

Project description:Wnt5a-YAP signaling axis mediates mechanotransduction in cardiac myocytes and contributes to the transition to heart failure (rat sample)

| PRJNA825767 | ENA

Wnt5a-YAP signaling axis mediates mechanotransduction in cardiac myocytes and contributes to the transition to heart failure

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

2023-07-17 | GSE200667 | GEO

Response of podocytes to PAN - YAP-mediated mechanotransduction determines the podocyte's response to damage

Project description:Podocytes are terminally differentiated cells at the kidney filtration barrier and exposed to considerable mechanical strain. Podocyte injury causes morphological changes as a result of cytoskeletal reorganizations and failure of the filtration barrier. The transcriptional co-activators YAP/TAZ are tightly controlled through hippo signaling and responsive to mechanical cues. Here, we show that YAP is upregulated upon podocyte injury to activate YAP-dependent target genes. This activation preceded the development of proteinuria. In contrast, similar perturbations of cells in culture did not reveal increased YAP activity but showed a downregulation of YAP/TAZ activity when cells were grown on stiff surface. However, culture of cells on soft matrix or inhibition of stress fiber formation allowed recapitulation of the damage-induced YAP upregulation indicating a mechanotransduction-dependent mechanism of YAP over-activity. Interestingly, increased expression of YAP targets was confirmed in renal biopsies from patients with glomerular disease. Consistently, pharmacological inhibition of YAP/TEAD activity ameliorated glomerular disease in vivo. These data suggest that perturbation of the mechanosensitive hippo signaling pathway may be a therapeutic principle in podocyte disease.

2017-04-19 | PXD003872 | Pride

Regulation of YAP Promotor Accessibility in Endothelial Mechanotransduction

Project description:Regulation of YAP Promotor Accessibility in Endothelial Mechanotransduction

| PRJNA1066889 | ENA

CCM3 is a gatekeeper in focal adhesions regulating mechanotransduction and YAP/TAZ signalling

Project description:We report that loss of CCM3/PDCD10 in fibroblasts induces FAK/Src-paxillin signalling driving actomyosin-dependent mechanotransduction leading to YAP/TAZ signalling. In vivo, loss of CCM3 in fibroblasts drives excessive tissue remodelling leading to the dissemination of breast cancer cells to distant organs.

2021-05-06 | GSE155688 | GEO

Caveolin-1 modulates mechanotransduction responses to substrate stiffness through actin-dependent control of YAP

Project description:The transcriptional regulator YAP orchestrates important cell functions, determining tissue homeostasis, organ growth control, and tumorigenesis. Mechanical stimuli are a key input to YAP activity, but the mechanisms controlling this regulation remain largely uncharacterized. We show that CAV1 positively modulates the YAP mechanoresponse to substrate stiffness through actin cytoskeleton-dependent and Hippo kinase-independent mechanisms. RHO activity is necessary but not sufficient for CAV1-dependent mechanoregulation of YAP activity. Systematic quantitative interactomic studies and image-based siRNA screenings provide evidence that this actin-dependent regulation is determined by YAP interaction with the 14-3-3 protein YWHAH. Constitutive YAP activation rescued phenotypes associated with CAV1 loss, including defective ECM remodeling. CAV1-mediated control of YAP activity was validated in vivo in a model of pancreatitis-driven acinar-to-ductal metaplasia. We propose that this CAV1-YAP mechanotransduction system controls a significant share of cell programs linked to these two pivotal regulators, with potentially broad physiological and pathological implications.

2018-10-16 | GSE120514 | GEO

UPLC-MS/MS of YAP co-IP during activating and inactivating plating conditions

Project description:To identify YAP binding partners potentially involved in mechanotransduction, we performed a YAP co-IP/MS experiment using sparsely or densely plated MCF10A cells.

2019-11-21 | PXD007287 | Pride

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