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 | GSE207491 | 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:Targeting the Alk4 pathway protects against age-related bone loss.
| PRJNA1400033 | ENA
Project description:Background: Mare milk is characterized by high nutritional value, good digestibility, and bioactive components with potential functional properties. However, dairy mares show marked individual variation in milk yield, and stable molecular indicators for identifying high-yielding individuals remain limited. Therefore, this study aimed to characterize molecular signatures associated with lactation-performance differences between high- and low-yielding dairy mares. Results: A total of 193 mid-lactation mares were enrolled, and 102 differential metabolites and 37 differentially expressed proteins were identified between high- and low-yielding mares. The differential molecules were mainly enriched in ABC transporters, glycine, serine and threonine metabolism, linoleic acid metabolism, focal adhesion, regulation of the actin cytoskeleton, redox homeostasis, and immune defense. Increased levels of Gly, 12,13-DiHOME, and 5-ALA in high-yielding mares suggested enhanced amino acid supply, lipid utilization, and mitochondrial-related energy metabolism, whereas changes in ARPC3, LAMP2, SEPTIN6, ST6GAL1, and MYL6 indicated potential involvement of cytoskeletal remodeling, lysosomal homeostasis, epithelial polarity, glycoprotein processing, and cell contraction. In cross-platform validation, Gly, 12,13-DiHOME, 5-ALA, ARPC3, PRDX2, LYZ, and LAMP2 exhibited relatively consistent differences and may serve as priority candidate molecules for further research. Conclusions: This study revealed serum multi-omics signatures associated with lactation-performance differences in dairy mares and highlighted candidate molecules related to nutrient metabolism, cytoskeletal remodeling, antioxidant defense, and immune regulation. These findings provide candidate biomarkers for early screening of high-yielding mares and offer insights into the molecular mechanisms underlying lactation performance in dairy horses
2026-07-21 | PXD080427 | Pride
Project description:The reverse transcriptase inhibitor 3TC protects against age-related cognitive dysfunction
| PRJNA882769 | ENA
Project description:The liver plays an important role in cardiovascular disease by amplifying systemic inflammation, while the underlying mechanisms remain to be defined. Soluble epoxide hydrolase (sEH) is a pro-inflammatory enzyme and pharmacological inhibition of sEH was shown to protect against various inflammatory diseases. In this study, we have identified a novel role of the liver, through expression of sEH, in the pathogenesis of abdominal aortic aneurysm (AAA). sEH expression and activity were markedly higher in mouse liver compared with aorta and further increased in the context of AAA. Pharmacological inhibition or hepatocyte-specific disruption of sEH prevented AAA formation in two animal models of AAA (systemic angiotensin II infusion and local aortic calcium chloride application), concomitant with reduced expression of complement C3 and serum amyloid A, liver-derived inflammatory factors causally linked to AAA formation. Interestingly, data from co-incubation of liver ex vivo with aorta identified galectin-3 secreted from the aneurysm-prone aorta that activate sEH in the liver. We also determined 12,13- dihydroxyoctadecenoic acid (DiHOME) and various circulating pro-inflammatory cytokines as a downstream mechanism potentially associated with hepatic sEH in the context of AAA. These novel findings provide direct evidence that bidirectional crosstalk between aorta and liver contributes to AAA via hepatic sEH.
2026-04-07 | PXD073197 | 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