Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1071672 | ENA |
REPOSITORIES: ENA
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Project description:Following the identification of a critical time window of Blood Brain Barrier formation in the mouse embryo, we aimed to identify genes important for barriergenesis. To this end, we isolated cortical and lung E13.5 endothelial cells and compared expression between the two populations. The working hypothesis was that endothelial cells which are actively building a barrier would have a uniqe pattern of gene expression that would be detectable in comparison to a non-barrier endothelial population that is also active in vasculogenesis. E13.5 Tie2-GFP embryos were micro-dissected for cortex and lungs. Cortex tissue was carefully cleared of the meninges and choroid plexus. FACS purification of GFP positive cells and GeneChip analysis was applied . All material from a single litter (10-13 embryos) was pooled and considered as a biological replicate. n=4 litters.
2014-05-14 | E-GEOD-56777 | biostudies-arrayexpress
Project description:Following the identification of a critical time window of Blood Brain Barrier formation in the mouse embryo, we aimed to identify genes important for barriergenesis. To this end, we isolated cortical and lung E13.5 endothelial cells and compared expression between the two populations. The working hypothesis was that endothelial cells which are actively building a barrier would have a uniqe pattern of gene expression that would be detectable in comparison to a non-barrier endothelial population that is also active in vasculogenesis.
2014-05-14 | GSE56777 | GEO
Project description:<h4><strong>BACKGROUND: </strong>Several studies have shown a correlation between an altered metabolome and respiratory allergies. The epithelial barrier hypothesis proposes that an epithelial barrier dysfunction can result in allergic diseases development. Der p 1 allergen from house dust mite is a renowned epithelial barrier disruptor and allergy initiator due to its cysteine-protease activity. Here, we compared the metabolic profile of the bronchial epithelium exposed or not to Der p 1 during barrier establishment to understand its active role in allergy development.</h4><h4><strong>METHODS: </strong>Calu-3 cells were cultivated in air-liquid interface cultures and exposed to either Der p 1 or Ole e 1 allergens during barrier establishment. The comparative metabolomics analysis of apical and basolateral media were performed using liquid chromatography and capillary electrophoresis both coupled to mass spectrometry.</h4><h4><strong>RESULTS: </strong>We showed that epithelial barrier disruption by Der p 1 was associated with a specific metabolic profile, which was highly dependent on the state of the epithelium at the time of contact. Moreover, an apical-basolateral distribution of the metabolites was also observed, indicating a compartmentalization of the response with differential metabolic patterns. A number of metabolites were changed by Der p 1, mainly related to amino acids metabolism, such as L-arginine, L-kynurenine and L-methionine.</h4><h4><strong>CONCLUSION: </strong>This work is the first report on the metabolic response in human bronchial epithelial cells associated with cysteine-protease Der p 1 activity, which could contribute to allergy development. Moreover, it supports a reformulated epithelial barrier hypothesis that might help to explain allergies and their increasing prevalence.</h4>
2023-08-22 | MTBLS1755 | MetaboLights
Project description:The loss of loricrin, a major component of the cornified envelope, results in a delay of epidermal barrier formation. Therefore, the living layers of the epidermis are aberrantly exposed to late-stage amniotic fluid, which may serve as the signal to upregulate genes that functionally compensate for the loss of loricrin. Consistent with this hypothesis, metabolomic studies revealed marked changes in amniotic fluid between E14.5 and E16.5 dpc. In addition, we discovered that the Nrf2/Keap1 pathway detects these compositional changes and directly upregulates the expression of genes involved in the compensatory response, thus ensuring postnatal survival. In support of this finding, we demonstrate that genetically blocking the Nrf2 pathway abolishes the compensatory response, and preemptively activating Nrf2 pharmacologically rescues the delay in barrier formation in utero. Our findings reveal that the functions of Nrf2 and the composition of amniotic fluid have co-evolved to ensure the formation of a functional barrier. 1 sample with one replicate for each genotype was performed for both loricrin knockout and wildtype
2013-06-28 | E-GEOD-41742 | biostudies-arrayexpress
Project description:As a type of secreted membrane vesicle, exosomes are emerging as an important mode of cell-to-cell communication. The objective of this study was to compare the abundance of mRNA and miRNA present in the parental B16F0 cell to mRNA and miRNA present in exosomes isolated from B16F0 conditioned media. Identifying local mechanisms of immunosuppression is a key barrier for expanding the clinical benefit of cancer immunotherapy. While exosomes are emerging as a new mode of intercellular communication, their role in establishing a malignant tissue niche remains unclear. Similar to the sculpting of tumor antigens during oncogenesis, a related hypothesis is that proteins secreted by malignant cells are shaped by somatic evolution. To test this hypothesis, we characterized the biological influence of tumor-derived exosomes on immune cell function.
2019-08-01 | GSE102883 | GEO
Project description:Immune cells regulate a hypertonic microenvironment in the skin; however, possible functions of increased skin Na+ concentrations are unknown. We found that Na+ accumulated at the site of bacterial skin infections in humans and in mice. We used the protozoan parasite Leishmania (L.) major as a model of skin-prone macrophage infection to test the hypothesis that skin-Na+ storage facilitates antimicrobial host defense. Activation of macrophages in the presence of high NaCl concentrations modified epigenetic markers and enhanced p38 mitogen-activated protein kinase (p38/MAPK)-dependent nuclear factor of activated T cells 5 (NFAT5) activation. This high-salt response resulted in elevated type-2 nitric oxide synthase (Nos2)-dependent NO production and improved L. major elimination. Finally, we found that increasing Na+ content in the skin by a high-salt diet boosted activation of macrophages in an Nfat5-dependent manner and promoted cutaneous antimicrobial defense. We suggest that the hypertonic microenvironment could serve as a barrier to infection.
2015-02-26 | E-MTAB-3343 | biostudies-arrayexpress
Project description:Active immunotherapy is a promising strategy for anti-angiogenic cancer therapy. Recently, we have reported that a vaccine using human umbilical vein endothelial cells (HUVECs) induced specific anti-endothelial immune responses in the most of immunized patients, and resulted in tumor regression in some patients with recurrent malignant brain tumors, whereas not in colorectal cancer patients. In this study, we hypothesized that non-hypoxic perivascular tumor associated macrophages (TAMs) in colorectal cancer, but not in glioblastoma, might negatively alter the therapeutic efficacy of anti-angiogenic active immunotherapy. To test this hypothesis, we examined global gene expression profiles of non-hypoxic macrophages stimulated in vitro by soluble factors released from tumor cells of human glioblastoma U-87MG (‘brain TAMs’) or colorectal adenocarcinoma HT-29 (‘colon TAMs’).
2012-04-01 | GSE18804 | GEO
Project description:Hypoxia-related pregnancy complications increase the risk of disease in the child in later life. No prevention is available. Previously we noted that a trophoblast barrier, an in vitro model of the placenta, reacted to oxidative stress by secreting factors that damage neighbouring cells. Application of mitochondrion-targeted antioxidant MitoQ prevented this. Here we tested the effects of MitoQ-bound nanoparticles on trophoblast barriers and in a rat model of gestational hypoxia.A single dose of MitoQ-nanoparticles, administered maternally before a hypoxic episode, reduced oxidative stress in the placental barrier without reaching the fetus and prevented changes to birthweight. MitoQ-nanoparticles further suppressed damaging signalling from the placental barriers. Altered signalling molecules in the fetal plasma and in conditioned media from rat placenta included changes to proteins with relevance to cardiovascular disease. We suggest as a future possibility, treatment of the placenta to prevent disease in the offspring in later life.
2017-08-22 | PXD004956 | Pride
Project description:Hypoxia-related pregnancy complications increase the risk of disease in the child in later life. No prevention is available. Previously we noted that a trophoblast barrier, an in vitro model of the placenta, reacted to oxidative stress by secreting factors that damage neighbouring cells. Application of mitochondrion-targeted antioxidant MitoQ prevented this. Here we tested the effects of MitoQ-bound nanoparticles on trophoblast barriers and in a rat model of gestational hypoxia.A single dose of MitoQ-nanoparticles, administered maternally before a hypoxic episode, reduced oxidative stress in the placental barrier without reaching the fetus and prevented changes to birthweight. MitoQ-nanoparticles further suppressed damaging signalling from the placental barriers. Altered signalling molecules in the fetal plasma and in conditioned media from rat placenta included changes to proteins with relevance to cardiovascular disease. We suggest as a future possibility, treatment of the placenta to prevent disease in the offspring in later life.
2017-08-22 | PXD004955 | Pride
Project description:For the formation of the blood-brain barrier not only endothelial cells alone, but also their interaction with surrounding cell types, like pericytes, plays an important role, and co-culture of the two cell types increases barrier function in vitro. Furthermore, observed sex differences with regard to several cardiovascular as well as neurodegenerative disorders have led to the hypothesis that the female sex hormone estrogen might protect from endothelial barrier break-down. Microarray analysis was performed to determine the effect of co-culture on the gene expression profiles of pericytes and endothelial cells. Additionally, cells were treated with and without estradiol in order to determine possible effects of the sex hormone on the two cell types in mono- and co-cultures.
2021-04-19 | GSE168514 | GEO