Differential Expression Profile of MicroRNAs and Tight Junction in Lung Tissue of Rat with Mitomycin-C Induced Pulmonary Veno-Occlusive Disease
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PROVIDER: PRJNA781468 | ENA |
REPOSITORIES: ENA
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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
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
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
2010-04-11 | GSE15492 | GEO
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
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
Project description:Tight junctions (TJs) are cell-cell adhesion structures that function as barriers between epithelial cells to avoid dehydration, regulate ion permeability and prevent invasion of bacteria and viruses. Disruption of TJs is causative of various inflammatory diseases including inflammatory bowel diseases (IBD), atopic dermatitis and asthma. We identified TJ-inducing small peptides from mouse peritoneum-conditioned medium. The peptides, which we designate junction-inducing peptide like a zipper (Jipper), are 35-40 residue peptides corresponding to the C-terminal region of alpha1-antitrypsin (A1AT), the serine protease inhibitor abundant in circulating blood. Both mouse and human synthetic Jippers, as well as the human A1AT C-terminal peptides cleaved by matrix metalloproteinases (MMPs), induces TJs at cell-cell boundary of epithelial cells. Our study identifies the TJ-inducing peptides in mammalian tissues, and provides a basis for a clinically relevant strategy against TJ barrier-disrupted diseases.
2020-06-28 | PXD014424 | JPOST Repository
Project description:Background: The initial formation of follicular antrum (iFFA) is a milestone in folliculogenesis, which serves as a boundary between gonadotropin (GTH) -independent folliculogenesis and GTH-dependent folliculogenesis and endows the follicle's ability to acquire response to GTHs and continue to survive. However, iFFA is a barren field in folliculogenesis research, which do not match its physiological significance. Methods:In this study, transcriptome sequencing was used to comprehensively analyze the changes in the life activities of cells in the ovary during iFFA, and then the regulatory mechanism of iFFA was deduced based on the results of omics analysis, and it was systematically verified by experiments. Result: Herein, we conducted in vivo and in vitro experiments to studied iFFA in a mouse model, and revealed that: (1) iFFA is a physiological process of active cell proliferation, increased energy expenditure, enhanced secretory activity and increased moisture absorption, accompanied by complex changes in epigenetic modification, bioclock regulation, and cell junctions; (2) iFFA and blastocoel formation may be conservatively regulated in fluid accumulation, and tight junctions, ion pumps and aquaporins underlie the structural, kinetic and transport foundations for fluid accumulation during iFAA, respectively; (3) mTOR-CNP is the main signal cascade regulating iFFA, it initiated iFFA by targeting tight junction/ion pumps/aquaporins and follicular cell proliferation; (4) FSH controls iFFA by targeting the intra-ovarian mTOR-CNP cascade; (5) mTOR activator could be used as an improver to increase the efficiency of in vitro follicular culture technology. Conclusion: Overall, this study elucidated the changes in follicular cells' life activities in preparation for iFFA, proposed the model of "Dam-Pump-Pipe" to explain the accumulation of follicular fluid, and confirmed that FSH-mTOR-CNP-Tight junction/Ion pumps/Aquaporins is the core cascade controlling iFFA. These findings would help to fill in the gaps in iFFA research, and enrich the theory of folliculogenesis regulation.
2023-12-31 | GSE207958 | GEO
Project description:Proteasome inhibitors are important chemotherapeutics in the treatment of multiple myeloma, but they are currently used empirically as no markers of sensitivity have been validated. We have identified expression of tight junction protein (TJP) 1 as being associated with sensitivity of plasma cells in vitro and in vivo to proteasome inhibitors. TJP1 suppressed expression of genes in the major histocompatibility class II region, including two catalytically active immunoproteasome subunits, thereby decreasing proteasome activity, a critical determinant of proteasome inhibitor sensitivity. This occurred through suppression by TJP1 of signaling through the epidermal growth factor receptor/Janus kinase 1/signal transducer and activator of transcription 3 pathway. In the clinic, high TJP1 expression in myeloma patients was associated with a significantly higher likelihood of responding to bortezomib, and with a longer time-to-progression after treatment. Taken together, these data support the use of TJP1 as a biomarker of sensitivity and resistance to proteasome inhibitors. To further elucidate mechanisms of bortezomib resistance, we developed human-derived multiple myeloma cell lines with a 4-fold or greater resistance to bortezomib. Then total RNA for bortezomib resistant (BR) and wild type (WT) was extracted and used for comparison by gene expression profiling.
2015-12-31 | E-GEOD-52369 | biostudies-arrayexpress
Project description:The mucosal epithelium plays a key role in regulating immune homeostasis. Dysregulation of epithelial barrier function is associated with mucosal inflammation. Expression of claudin-2, a pore-forming tight junction protein, is highly upregulated during inflammatory bowel disease (IBD) and, due to its association with epithelial permeability, has been postulated to promote inflammation. Furthermore, claudin-2 also regulates colonic epithelial cell proliferation and intestinal nutrient absorption. However, the precise role of claudin-2 in regulating colonic epithelial and immune homeostasis remains unclear. Here, we demonstrate, using Villin-Claudin-2 transgenic (Cl-2TG) mice, that increased colonic claudin-2 expression unexpectedly protects mice against experimentally induced colitis and colitis-associated cancer. Notably, Cl-2TG mice exhibited increased colon length and permeability as compared with wild type (WT) littermates. However, despite their leaky colon, Cl-2TG mice subjected to experimental colitis were immune compromised, with reduced induction of TLR-2, TLR-4, Myd-88 expression and NF-kB and STAT3 activation. Most importantly, colonic macrophages in Cl-2TG mice exhibited an anergic phenotype. Claudin-2 overexpression also increased colonocyte proliferation and provided protection against colitis-induced colonocyte death. Taken together, our findings have revealed a critical role of claudin-2 in regulating colonic homeostasis, suggesting novel therapeutic strategies for inflammatory conditions of the gastrointestinal tract. 8-10 weeks old male Villin-Claudin-2 transgenic mice and WT littermates were provided either normal drinking water (control) or Dextran Sodium Sulfate (DSS: 4% w/v) for 10 days. 3 replicates each.
2013-09-15 | E-GEOD-46006 | biostudies-arrayexpress
Project description:Proteasome inhibitors are important chemotherapeutics in the treatment of multiple myeloma, but they are currently used empirically as no markers of sensitivity have been validated. We have identified expression of tight junction protein (TJP) 1 as being associated with sensitivity of plasma cells in vitro and in vivo to proteasome inhibitors. TJP1 suppressed expression of genes in the major histocompatibility class II region, including two catalytically active immunoproteasome subunits, thereby decreasing proteasome activity, a critical determinant of proteasome inhibitor sensitivity. This occurred through suppression by TJP1 of signaling through the epidermal growth factor receptor/Janus kinase 1/signal transducer and activator of transcription 3 pathway. In the clinic, high TJP1 expression in myeloma patients was associated with a significantly higher likelihood of responding to bortezomib, and with a longer time-to-progression after treatment. Taken together, these data support the use of TJP1 as a biomarker of sensitivity and resistance to proteasome inhibitors.
2015-12-31 | GSE52369 | GEO