Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1291650 | ENA |
REPOSITORIES: ENA
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Project description:Elevated infant fecal concentrations of bacterial-derived lipid 12,13-diHOME increases risk for atopy and asthma development in childhood, mechanistically how this lipid may contribute to disease susceptibility is unknown. Here we demonstrate macrophages exposed to 12,13-diHOME exhibit inflammatory IL-1bhighCD206low M1-like polarization, reduce bacterial phagocytic capacity. In co-culture assays, antigens in the presence of 12,13-diHOME further amplifies M1-like frequency, promotes CD20+CD38-IgD-CD27+ memory B cells expansion and IgE production. Epigenetic analyses indicates 12,13-diHOME exposure promotes DNA methylation, chromatin compaction, specifically diminishing access to interferon-stimulated response elements and transcription factor binding sites. In vivo, in murine airway allergic sensitization model, gut bacterial-derived 12,13-diHOME exacerbated both airway allergic inflammation and IL-1, IL-7, one-carbon metabolism and Toll-like receptor signaling. Our data suggests that 12,13-diHOME reprograms macrophage effector function, B-cell interactions and epigenetic modifications promoting phenotypes plausibly play a role in shaping early life microbiome development and innate immune dysfunction related to allergic sensitization in childhood.
2022-07-08 | GSE207492 | GEO
Project description:Elevated infant fecal concentrations of bacterial-derived lipid 12,13-diHOME increases risk for atopy and asthma development in childhood, mechanistically how this lipid may contribute to disease susceptibility is unknown. Here we demonstrate macrophages exposed to 12,13-diHOME exhibit inflammatory IL-1highCD206low M1-like polarization, reduce bacterial phagocytic capacity. In co-culture assays, antigens in the presence of 12,13-diHOME further amplifies M1-like frequency, promotes CD20+CD38-IgD-CD27+ memory B cells expansion and IgE production. Epigenetic analyses indicates 12,13-diHOME exposure promotes DNA methylation, chromatin compaction, specifically diminishing access to interferon-stimulated response elements and transcription factor binding sites. In vivo, in murine airway allergic sensitization model, gut bacterial-derived 12,13-diHOME exacerbated both airway allergic inflammation and IL-1, IL-7, one-carbon metabolism and Toll-like receptor signaling. Our data suggests that 12,13-diHOME reprograms macrophage effector function, B-cell interactions and epigenetic modifications promoting phenotypes plausibly play a role in shaping early life microbiome development and innate immune dysfunction related to allergic sensitization in childhood.
2022-07-08 | GSE207528 | GEO
Project description:Elevated infant fecal concentrations of bacterial-derived lipid 12,13-diHOME increases risk for atopy and asthma development in childhood, mechanistically how this lipid may contribute to disease susceptibility is unknown. Here we demonstrate macrophages exposed to 12,13-diHOME exhibit inflammatory IL-1highCD206low M1-like polarization, reduce bacterial phagocytic capacity. In co-culture assays, antigens in the presence of 12,13-diHOME further amplifies M1-like frequency, promotes CD20+CD38-IgD-CD27+ memory B cells expansion and IgE production. Epigenetic analyses indicates 12,13-diHOME exposure promotes DNA methylation, chromatin compaction, specifically diminishing access to interferon-stimulated response elements and transcription factor binding sites. In vivo, in murine airway allergic sensitization model, gut bacterial-derived 12,13-diHOME exacerbated both airway allergic inflammation and IL-1, IL-7, one-carbon metabolism and Toll-like receptor signaling. Our data suggests that 12,13-diHOME reprograms macrophage effector function, B-cell interactions and epigenetic modifications promoting phenotypes plausibly play a role in shaping early life microbiome development and innate immune dysfunction related to allergic sensitization in childhood.
2022-07-08 | GSE207491 | GEO
Project description:Targeting the Alk4 pathway protects against age-related bone loss.
| PRJNA1400033 | ENA
Project description:The reverse transcriptase inhibitor 3TC protects against age-related cognitive dysfunction
| PRJNA882769 | ENA
Project description:Molecular characterization of medulloblastoma (MB) cell origin and properties is the basis for a well-defined classification system. However, limited data is available regarding the MB tumor microenvironment. Here we present a mass spectrometry-based multi-omics study of cerebrospinal fluid (CSF) from recurrent MB patients. A group of age-matched patients without a neoplastic disease was used as control cohort. Proteome profiling identified several characteristic tumor markers and revealed a strong prevalence of anti-inflammatory and tumor-promoting proteins characteristic for alternatively polarized myeloid cells in MB samples. The up-regulation of ADAMTS1, GAP43 and GPR37 indicated hypoxia in CSF of MB patients. This notion was independently supported by metabolomics, demonstrating up-regulation of tryptophan, methionine, serine and lysine, all of which have been described to be induced upon hypoxia in CSF. The beta-oxidation promoting lipid hormone 12,13-DiHOME was found strongly upregulated, potentially promoting a metabolic shift supporting drug resistance and stem cell properties of MB cells.
2020-06-01 | PXD018226 | Pride
Project description:This SuperSeries is composed of the following subset Series: GSE24992: Drosophila brain microRNA expression with age: miRNA profiling GSE25007: Drosophila brain gene expression with age: mRNA profiling GSE25008: Drosophila brain gene expression between wildtype and miR-34 null flies Refer to individual Series. Aging is the most prominent risk factor for human neurodegenerative disease, but underlying mechanisms that connect two processes are less well characterized. With age, the brain undergoes functional decline and perhaps degeneration. Such decline may not just contribute to normal aging, but also enhance susceptibility to and progression of age-related neurodegenerative diseases. Therefore, defining intrinsic factors and pathways that underline the normal integrity of the adult nervous system may lead to insights that potentially link aging and neurodegeneration. Here, we report a highly conserved microRNA (miRNA), miR-34, as a modulator of aging and neurodegeneration. Using Drosophila, we show that fly miR-34 expression is brain-enriched and strikingly upregulated with age. Functional studies reveal that, whereas animals without miR-34 are normal as young adults, upon aging, they gradually show late-onset deficits characteristic of accelerated brain aging; these include a transcriptional signature of aged animals, coupled with rapid functional decline, loss of brain integrity, followed by a catastrophic decline in adult viability. Moreover, upregulation of miR-34 protects against neurodegeneration induced by pathogenic human polyglutamine (polyQ) disease protein. We next reveal a dramatic effect of miR-34 to silence the Eip74EF gene of steroid hormone pathways in the adult, which is crucial to maintain the normal aging. Collectively, these data define a miR-34-mediated mechanism that specifically affects long-term integrity of the adult nervous system. miR-34 function in Drosophila may thus present a link that functionally connects aging and neurodegeneration. Our studies implicate essential roles of miRNA- dependent pathways in maintenance of the adult brain, disease pathogenesis and healthy aging.
2011-12-23 | E-GEOD-25009 | biostudies-arrayexpress
Project description:Age-related changes in cardiac homeostasis lead to myocardial dysfunction and cardiovascular diseases, which predict the healthspan of ageing. Age is a prominent risk factor for cardiac-related diseases. During ageing, the heart undergoes structural remodeling (increased cardiac weight and myocardial fibrosis) and functional decline (reduced diastolic and systolic functions), causing vulnerability of the heart to extra stress. Consequently, these pathological changes lead to increased cardiovascular mortality and morbidity in elderly adults. The underlying mechanism of cardiac ageing remains largely unexplored; and no pharmacological agent is currently available to improve or delay cardiac senescence.
2025-01-29 | GSE200741 | GEO
Project description:Age-related obesity is a growing public health concern linked to various metabolic disorders, yet its underlying mechanisms remain incompletely understood. Here we report that S-nitrosoglutathione reductase (GSNOR), a pivotal denitrosation enzyme, increases in adipose tissue of both male mice and humans from middle-age. GSNOR knockout protects against age-related weight gain and enhances metabolism, whereas adipose-specific GSNOR knock-in mice promotes obesity and metabolic decline. Further investigation reveals that aged GSNOR KO mice maintain higher mitochondrial content and more beige adipocytes, whereas adipose-specific GSNOR overexpression promotes adipose tissue whitening. Mechanistically, GSNOR denitrosates Beclin-1 at cysteine 351 and mutation of this site (Beclin-1C351A) increases autophagy by enhancing Beclin-1 and ATG14 interaction, thereby accelerating beige-to-white adipocyte conversion. Together, our findings reveal that GSNOR regulates adipose tissue remodeling during aging through Beclin-1 S-nitrosation, pointing to a potential therapeutic target for age-related obesity.
2026-01-26 | GSE317377 | GEO