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Tight Junction Claudins-associated vascular heterogeneity determines organotypic metastasis

ABSTRACT: Tight Junction Claudins-associated vascular heterogeneity determines organotypic metastasis

PROVIDER: PRJNA818702 | ENA |

REPOSITORIES: ENA

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Tight Junction Claudins-associated vascular heterogeneity determines organotypic metastasis

Project description:To identify the underlying mechanisms associated with lung and kidney fibrosis inducing lung metastasis, we evaluated global transcriptomic changes in healthy lung, fibrotic lung fibrosis, and lung from mice with kidney fibrosis. Results provide information on the vascular remodeling of the lungs with organ fibrosis. Lung fibrosis is induced with intratracheal bleomycin administration. Kidney fibrosis is induced by unilateral ureter obstruction (UUO).

2024-04-19 | GSE199178 | GEO

Clostridioides difficile toxins deregulate tight junction proteins.

Project description:Clostridioides difficile toxins deregulate tight junction proteins.

| PRJNA973611 | ENA

Membrane prewetting by condensates promotes tight junction belt formation

Project description:Time-resolve proximity proteomics of tight junction. To understand how the tight junction belt is assembled and positioned, we combined APEX2 proximity proteomics of the main junctional scaffold protein ZO-1 with a calcium switch tissue formation assay.This combination allowed us to synchronize the initiation of junction assembly in the entire tissue by the addition of calcium to the culture medium and quantify the time evolution of the junctional proteome during the assembly process using proximity proteomics.

2024-05-22 | PXD052221 | Pride

Hypoxia inducible microRNA-155 negatively regulates epithelial barrier in Eosinophilic Esophagitis by suppressing Tight Junction Claudin-7

Project description:MicroRNA (miRNA)-mediated mRNA regulation directs many homeostatic and pathological processes, but how miRNAs coordinate aberrant esophageal inflammation during eosinophilic esophagitis (EoE) is poorly understood. Here, we report a deregulatory axis where microRNA-155 (miR-155) regulates epithelial barrier dysfunction by selectively constraining tight junction CLDN7 (claudin-7). MiR-155 is elevated in the esophageal epithelium of biopsies from patients with active EoE and in cell culture models. miR-155 localisation using in situ hybridisation (ISH) in patient biopsies, and intra-epithelial compartmentalisation of miR-155 shows expression predominantly within the basal epithelia. Epithelial miR-155 activity was evident through diminished target gene expression in 3D organotypic cultures, particularly in relatively undifferentiated basal cell states. Mechanistically, generation of a novel cell line with enhanced epithelial miR-155 stable overexpression induced a functionally deficient epithelial barrier in 3D air-liquid interface epithelial cultures measured by transepithelial electrical resistance (TEER). Histological assessment of 3D esophageal organoid cultures overexpressing miR-155 showed notable dilated intra-epithelial spaces. Unbiased RNA-sequencing analysis and immunofluorescence determined a defect in epithelial barrier tight junctions and revealed a selective reduction in the expression of critical esophageal tight junction molecule, claudin-7. Together, our data reveal a previously unappreciated role for miR-155 in mediating epithelial barrier dysfunction in esophageal inflammation.

2023-12-12 | GSE244629 | GEO

Differential Expression Profile of MicroRNAs and Tight Junction in Lung Tissue of Rat with Mitomycin-C Induced Pulmonary Veno-Occlusive Disease

Project description:Pulmonary veno-occlusive disease (PVOD) is characterized by increased pulmonary vascular resistance. Currently, there is a lack of effective treatment. It is of great significance to explore molecular targets for treatment of the disease. This study investigated the differentially expressed profile of miRNAs and tight junction in the lung tissue of rats with mitomycin-C induced PVOD.

2021-11-30 | GSE189080 | GEO

Functional analysis of membrane-associated scaffolding tight junction (TJ) proteins in tumorigenic characteristics of B16-F10 mouse melanoma cells.

Project description:Tight junction (TJ) proteins (Tjps), Tjp1 and Tjp2, are tight junction-associated scaffold proteins that bind to the transmembrane proteins of tight junctions and the underlying cytoskeleton. In this study, we first analyzed the tumorigenic characteristics of B16-F10 melanoma cells, including cell proliferation, migration, invasion, metastatic potential, and the expression patterns of related proteins, after the CRISPR-Cas9-mediated knockout (KO) of Tjp genes. The proliferation of Tjp1 and Tjp2 KO cells significantly increased in vitro. Other tumorigenic characteristics, including migration and invasion, were significantly enhanced in Tjp1 and Tjp2 KO cells.

2024-08-01 | GSE240070 | GEO

Loss of tight junction integrity induces loss of epithelial phenotype: case of Claudin11 knock out in testis.

2010-04-11 | GSE15492 | GEO

Loss of tight junction integrity induces loss of epithelial phenotype: case of Claudin11 knock out in testis.

Project description:Epithelium barrier integrity is assumed at least in part by the presence of junctions between cells. Tight-junction formation may be necessary for Sertoli cells to cease dividing and to support germ cell development. Microarray analysis of P20 Cldn11 +/- and Cldn11-/- testes confirmed the impact od Cldn11 deficiency on cell cytoskeleton and junction-related genes. Keywords: transcriptomic analysis Two-condition experiment: P20 Cldn11 +/- vs. P20 Cldn11 -/- testes. A pool of RNA from P20 Cldn11 +/- group was used as the reference group. Each P20 Cldn11 -/- was compared to reference group. Three biological replicates were processed in dye swap.

2010-04-11 | E-GEOD-15492 | biostudies-arrayexpress

Dietary Gluten-Induced Gut Dysbiosis is Accompanied by Selective Upregulation of microRNAs with Intestinal Tight Junction and Bacteria-Binding Motifs in Rhesus Macaque Model of Celiac Disease

Project description:The study describes miRNA expression in intact jejunum following feeding of gluten containing monkey chow to gluten sensitive (GS) rhesus macaques. Gluten feeding induced several inflammation associated miRNAs validated and predicted to directly target intestinal tight junction proteins. Upregulation of these microRNAs was accompanied significantly reduced mRNA expression of claudin-1, claudin-3 and occludin and severe gut dysbiosis. These findings suggest that miRNA mediated downregulation of intestinal epithelial tight junction proteins could increase intestinal permeability and facilitate translocation of dysbiotic bacteria into the systemic circulation.

2016-11-10 | GSE89170 | GEO

HEK NICD AP-MS - Notch signaling is a core patterning module for vascular morphogenesis, which co-determines the sprouting behaviour of endothelial cells (ECs)

Project description:Notch signaling is a core patterning module for vascular morphogenesis, which co-determines the sprouting behaviour of endothelial cells (ECs). Tight quantitative and temporal control of Notch activity is essential for vascular development, yet the details of Notch regulation in ECs are incompletely understood. We found that ubiquitin-specific peptidase 10 (USP10) interacted with the NOTCH1 intracellular domain (NICD1) to slow the ubiquitin-dependent turnover of this short-lived form of the activated NOTCH1 receptor. Accordingly, inactivation of USP10 reduced NICD1 abundance and stability, and diminished Notch-induced target gene expression in ECs. In mice, loss of endothelial Usp10 increased vessel sprouting and partially restored the patterning defects caused by ectopic expression of NICD1. Thus, USP10 functions as an NICD1 deubiquitinase, which fine-tunes endothelial Notch responses during angiogenic sprouting.

2019-04-11 | PXD013192 | Pride

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