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Wnt5a–Vangl1/2 signaling regulates the position and direction of lung branching through the cytoskeleton and focal adhesions

ABSTRACT: Wnt5a–Vangl1/2 signaling regulates the position and direction of lung branching through the cytoskeleton and focal adhesions

PROVIDER: PRJNA780961 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16961000.fastq.gz	Fastqsanger.gz
	SRR16961001.fastq.gz	Fastqsanger.gz
	SRR16961002.fastq.gz	Fastqsanger.gz
	SRR16961003.fastq.gz	Fastqsanger.gz
	SRR16961004.fastq.gz	Fastqsanger.gz

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Similar Datasets

Wnt5a–Vangl1/2 signaling regulates the position and direction of lung branching through the cytoskeleton and focal adhesions

Project description:Lung branching morphogenesis requires reciprocal interactions between the epithelium and mesenchyme. How the lung branches are generated at a defined location and projected toward a specific direction remains a major unresolved issue. In this study, we investigated the function of Wnt signaling in lung branching in mice. We discovered that Wnt5a in both the epithelium and mesenchyme plays an essential role in controlling the position and direction of lung branching. The Wnt5a signal is mediated by Vangl1/2 to trigger a cascade of non-canonical or planar cell polarity (PCP) signaling. In response to non-canonical Wnt signaling, lung cells undergo cytoskeletal reorganization and change focal adhesions. Perturbed focal adhesions in lung explants are associated with defective branching. Moreover, we observed changes in the shape and orientation of the epithelial sheet and the underlying mesenchymal layer in regions of defective branching in the mutant lungs. Thus, PCP signaling helps define the position and orientation of the lung branches. We propose that mechanical force induced by non-canonical Wnt signaling mediates a coordinated alteration in the shape and orientation of a group of epithelial and mesenchymal cells. These results provide a new framework for understanding the molecular mechanisms by which a stereotypic branching pattern is generated.

2022-07-10 | GSE188993 | GEO

Wnt5a-Vangl1/2 signaling regulates the position and direction of lung branching through the cytoskeleton and focal adhesions.

Project description:Lung branching morphogenesis requires reciprocal interactions between the epithelium and mesenchyme. How the lung branches are generated at a defined location and projected toward a specific direction remains a major unresolved issue. In this study, we investigated the function of Wnt signaling in lung branching in mice. We discovered that Wnt5a in both the epithelium and the mesenchyme plays an essential role in controlling the position and direction of lung branching. The Wnt5a signal is mediated by Vangl1/2 to trigger a cascade of noncanonical or planar cell polarity (PCP) signaling. In response to noncanonical Wnt signaling, lung cells undergo cytoskeletal reorganization and change focal adhesions. Perturbed focal adhesions in lung explants are associated with defective branching. Moreover, we observed changes in the shape and orientation of the epithelial sheet and the underlying mesenchymal layer in regions of defective branching in the mutant lungs. Thus, PCP signaling helps define the position and orientation of the lung branches. We propose that mechanical force induced by noncanonical Wnt signaling mediates a coordinated alteration in the shape and orientation of a group of epithelial and mesenchymal cells. These results provide a new framework for understanding the molecular mechanisms by which a stereotypic branching pattern is generated.

| S-EPMC9469998 | biostudies-literature

Wnt5a and Vangl1/2 signaling regulates the position and direction of lung branching through the cytoskeleton and focal adhesions

Project description:Whole cell proteomics on WT and VdKO cell lines prepared with preomics iST kit. 200 ng injections with 90 min gradient.

2022-07-08 | MSV000089851 | MassIVE

Wnt5A signaling in human coronary artery endothelial cells

Project description:Inflammatory Wnt5A signalling in human macrophages was found to be critically involved in severe systemic inflammatory response. However, the targets of Wnt5A in endothelial cells and downstream mechanisms by which Wnt5A might induce endothelial inflammation still remain unclear. We show that Wnt5A principally regulate genes involved endothelial cytoskeleton rearrangements and impairs the barrier function of cultured endothelial monolayer causing hyper permeability. We further prove that Wnt5A neither affects the expression of adhesion molecules nor induces cytokine storm in endothelial cells. These findings suggest that Wnt5A, secreted by activated macrophages during septic inflammation, paracrinically act on the endothelial wall, causing endothelial barrier breakdown and subsequent vascular leakage in sepsis.

2016-10-03 | GSE62281 | GEO

A mammalian Wnt5a–Ror2–Vangl2 axis controls the cytoskeleton and confers cellular properties required for alveologenesis

Project description:Alveolar formation increases the surface area for gas-exchange and is key to the physiological function of the lung. Alveolar epithelial cells, myofibroblasts and endothelial cells undergo coordinated morphogenesis to generate epithelial folds (secondary septa) within the saccules to form alveoli. A mechanistic understanding of alveologenesis remains incomplete. We found that the planar cell polarity (PCP) pathway is required in both alveolar epithelial cells and myofibroblasts for alveologenesis. Our studies uncovered a Wnt5a–Ror2–Vangl2 cascade that endows cellular properties and thus novel mechanisms of alveologenesis. This includes PDGF secretion from alveolar type I and type II cells, cell shape changes of type I cells and migration of myofibroblasts. All these cellular properties are conferred by changes in the cytoskeleton and represent a new facet of PCP function. These results extend our current model of PCP signaling from polarizing a field of epithelial cells to conferring new properties at subcellular levels to regulate collective cell behavior.

2020-03-03 | GSE140779 | GEO

A mammalian Wnt5a–Ror2–Vangl2 axis controls the cytoskeleton and confers cellular properties required for alveologenesis

Project description:A mammalian Wnt5a–Ror2–Vangl2 axis controls the cytoskeleton and confers cellular properties required for alveologenesis

| PRJNA590893 | ENA

Proinflammatory signaling mediated by the combined action of IL-1/Wnt5A in human coronary artery endothelial cells

Project description:IL-1b and Wnt5A are released from macrophages in systemic inflammation and sepsis. However, the early response targets for the paracrine action of synergistic interaction of IL-1b with Wnt5A in vascular endothelial cells still remain unclear. Here we show that IL-1b synergizes with Wnt5A to stimulate vascular endothelial inflammatory pathways involved in barrier dysfunction. Molecular targets involved in actin cytoskeleton remodeling, coagulation and stress signaling which are targets for known drugs are regulated by the synergistic action.

2021-06-09 | GSE146691 | GEO

HIF2 regulates intestinal Wnt5a expression

Project description:Radiation therapy for abdominal tumors is challenging because the small intestine is exquisitely radiosensitive. Unfortunately, there are no FDA-approved therapies to prevent or mitigate GI radiotoxicity. The EGLN protein family are oxygen sensors that regulate cell survival and metabolism through the degradation of hypoxia-inducible factors (HIFs). Our group has previously shown that stabilization of HIF2 through genetic deletion or pharmacologic inhibition of the EGLNs mitigates and protects against GI radiotoxicity in mice by improving intestinal crypt stem cell survival. Here we aimed to elucidate the molecular mechanisms by which HIF2 confers GI radioprotection. We developed duodenal organoids from mice, transiently overexpressed non-degradable HIF2, and performed bulk RNA sequencing. Interestingly, HIF2 upregulated known radiation modulators and genes involved in GI homeostasis, including Wnt5a. Non-canonical Wnt5a signaling has been shown by other groups to improve intestinal crypt regeneration in response to injury. Here we show that HIF2 drives Wnt5a expression in multiple duodenal organoid models. Luciferase reporter assays performed in human cells showed that HIF2 directly activates the WNT5A promoter via a hypoxia response element. We then evaluated crypt regeneration using spheroid formation assays. Duodenal organoids that were pre-treated with recombinant Wnt5a had a higher cryptogenic capacity after irradiation, compared to vehicle-treated organoids. Conversely, we found that Wnt5a knockout decreased the cryptogenic potential of intestinal stem cells following irradiation. Treatment with recombinant Wnt5a prior to irradiation rescued the cryptogenic capacity of Wnt5a knockout organoids, indicating that Wnt5a is necessary and sufficient for duodenal radioprotection. Taken together, our results.txt suggest that HIF2 radioprotects the GI tract by inducing Wnt5a expression.

2021-12-15 | GSE186927 | GEO

Wnt5a-deficient vs. wild-type E18 liver

Project description:Transcriptional profiling of E18.5 livers derived from Wnt5a-deficient (KO) mice compared to those from littermate wild-type (WT) mice. RNA samples were extracted from whole livers derived from E18.5 fetuses. Two-condition experiment: Wnt5a KO vs. WT whole livers. Total RNA samples were extracted from E18.5 whole livers. KO and WT samples were a mixture of RNA solutions derived from two Wnt5a KO livers and two WT livers, respectively.

2013-02-07 | E-GEOD-41803 | biostudies-arrayexpress

GPM6B regulates osteoblast differentiation and induction of mineralization by controlling cytoskeleton and matrix vesicle release.

Project description:Analysis of GPM6B silenced osteogenic hMSC at gene expression level. Analysis is showing significant changes in genes involved in cytoskeleton organization and biogenesis. Immunocytochemistry confirms changed distribution of actin filaments and change in shape and in size of focal adhesions upon GPM6B silencing. Moreover, we demonstrated that production and release of ALP-positive matrix vesicles (MVs) was reduced. In conclusion, we identified GPM6B as a novel regulator of osteoblast differentiation and bone formation and thereby demonstrating the significance of cytoskeleton organization for MV production and eventual mineralization.

2011-06-01 | GSE26004 | GEO

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