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Inflammation of gill epithelia in fish causes increased permeation of polar organic chemicals from OSPW via disruption of tight junctions

ABSTRACT: Inflammation of gill epithelia in fish causes increased permeation of polar organic chemicals from OSPW via disruption of tight junctions

PROVIDER: PRJNA758417 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15658200_1.fastq.gz	Fastqsanger.gz
	SRR15658200_2.fastq.gz	Fastqsanger.gz
	SRR15658201_1.fastq.gz	Fastqsanger.gz
	SRR15658201_2.fastq.gz	Fastqsanger.gz
	SRR15658202_1.fastq.gz	Fastqsanger.gz

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Inflammation of gill epithelia in fish causes increased permeation of polar organic chemicals from OSPW via disruption of tight junctions

Project description:The epithelial cell layer that lines the fish gill controls the paracellular permeation of chemicals through tight junctions. The integrity of tight junctions can be affected by inflammation, which is likely to impact the branchial bioavailability of chemicals. In this study, we experimentally induced inflammation in the rainbow trout gill cell line RTgill-W1 via exposure to bacterial lipopolysaccharides (LPS). We then co-exposed the cells to extracts of oil sands process-affected water (OSPW), which contain a complex mixture of toxicologically relevant chemicals. Cells exposed to LPS showed a significant reduction in transepithelial electrical resistance (TEER), an indicator of tight junction integrity, after 24 h of exposure. Quantitative RT-PCR analysis determined that the abundance of transcripts of genes coding for tight junction proteins (Claudin 28b and 10e) was significantly decreased in cells exposed to 20, 50, and 100 mg L-1 LPS. Chemical analysis revealed a significant increase in permeation of constituents of OSPW across the gill cell epithelial layer at all studied LPS concentrations. These in vitro findings were confirmed in vivo in rainbow trout fingerlings exposed to both LPS and 10% OSPW for 48 h, which similarly resulted in an increase in chemical uptake relative to fish exposed to OSPW alone. This research demonstrated that inflammation of gill epithelia and the resulting disruption of tight junction integrity could lead to significantly greater uptake of potentially harmful chemicals from the environment, which has important implications for risk assessment.

2022-02-28 | GSE182953 | GEO

Loss of tight junctions disrupts gastrulation patterning and increases differentiation towards the germ cell lineage in human pluripotent stem cells

Project description:To investigate the role of tight junctions in BMP4 signaling and differentiation, we knocked down TJP1 in human pluripotent stem cells using CRISPRi, and examined gene expression via RNA sequencing of TWT (no KD) and TKD (TJP1 KD) cells in the untreated pluripotent (P) state and after BMP4 differentiation (B).

2022-09-23 | GSE213911 | GEO

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

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 junctions disrupts gastrulation patterning and increases differentiation towards the germ cell lineage in human pluripotent stem cells

Project description:Loss of tight junctions disrupts gastrulation patterning and increases differentiation towards the germ cell lineage in human pluripotent stem cells

| PRJNA883000 | ENA

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

Proximity proteomics identifies PAK4 as a component of Afadin–Nectin junctions.

Project description:Human PAK4 is an ubiquitously expressed p21-activated kinase which acts downstream of Cdc42. Since PAK4 is demonstrably enriched in cell-cell junctions, we probed the local protein environment around the kinase with a view to understanding its location and substrates. In U2OS cells expressing PAK4-BirA-GFP the resultant SILAC proximity analyses revealed a subset of 28 proteins that are primarily cell-cell junction components. The protein with highest relative biotin labelling was Afadin/AF6, which associates with the nectin family of homophilic junctional proteins. Reciprocally >50% of the PAK4-proximal proteins were identified by Afadin BioID. Pull-down experiments failed to identify junctional proteins, emphasizing the advantage of the BioID method. Mechanistically PAK4 depended on Afadin for its junctional localization, which is similar to the situation in Drosophila. A highly ranked PAK4-proximal protein LZTS2 was immuno-localized with Afadin at cell-cell junctions. Though PAK4 and Cdc42 are junctional, BioID analysis did not yield conventional cadherins, indicating their spatial segregation. To identify cellular PAK4 substrates we then assessed changes in phospho-proteome after 12 min PF-3758309 treatment. Among the PAK4-proximal junctional proteins 17 PAK4 sites were identified. Thus we show PAK4 is selective for the mammalian Afadin/nectin sub-compartment, with a demonstrably distinct localization from tight and cadherin junctions.

2021-11-30 | PXD024464 | Pride

Embryonic exposure to aluminium chloride blocks the onset of spermatogenesis through disturbing the dynamics of testicular tight junctions via upregulating Slc25a5 in offspring

Project description:Embryonic exposure to aluminium chloride blocks the onset of spermatogenesis through disturbing the dynamics of testicular tight junctions via upregulating Slc25a5 in offspring

| PRJNA1011930 | ENA

ERK3 is essential for establishment of epithelial architecture [ERK3 KD vs. TFAP2A KD]

Project description:Establishment and maintenance of epithelial architecture are essential for embryonic development and adult physiology. Here, we show that ERK3, a poorly characterized atypical MAPK, regulates epithelial architecture in vertebrates. In Xenopus embryonic epidermal epithelia, ERK3 knockdown impairs adherens and tight junction protein distribution, as well as tight junction barrier function, resulting in epidermal breakdown. Moreover, in human breast epithelial cancer cells, inhibition of ERK3 expression induces thickened epithelia with aberrant adherens and tight junctions. Microarray results suggest an involvement of TFAP2A, a transcription factor important for epithelial gene expression, in ERK3-dependent gene expression changes. TFAP2A knockdown phenocopies ERK3 knockdown in both Xenopus embryos and human cells, and ERK3 is required for full activation of TFAP2A-dependent transcription. Our findings thus reveal that ERK3 regulates epithelial architecture, possibly in cooperation with TFAP2A. We used microarrays to compare the changes in ERK3-dependent gene expression profiles with those in TFAP2A-dependent gene expression profiles in Xenopus laevis embryos.

2018-06-13 | GSE110428 | GEO

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