Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA738512 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Antiviral response dictated by choreographed cascade of transcription factors
| PRJNA121193 | ENA
Project description:Age-related expression data from composite bone marrow from healthy humans
| PRJNA106327 | ENA
Project description:The gradual decline of tissue functionality is the main reason why humans suffer from age-related diseases. The prevalence for cardiovascular diseases increases with increasing age. In order to prevent age-related cardiac diseases, it is of importance to understand the respective age-associated risk factors. We have therefore compared the ventricular transcriptome of old and young hearts of the model organism zebrafish. We identified the immune system as activated in the old and found muscle organization to deteriorate upon aging. We show an accumulation of immune cells, mostly macrophages, in the old zebrafish ventricle.
2022-01-20 | GSE182979 | GEO
Project description:Mitochondrial dsRNA triggers antiviral signalling in humans
| PRJNA374913 | ENA
Project description:Protein translation (PT) declines with age in invertebrates, rodents, and humans. It has been assumed that elevated PT at young ages is beneficial to health and PT ends up dropping as a passive byproduct of aging. In Drosophila, we show that a transient elevation in PT during early-adulthood exerts long-lasting negative impacts on aging trajectories and proteostasis in later-life. Blocking the early-life PT elevation robustly improves life-/health-span and prevents age-related protein aggregation, whereas transiently inducing an early-life PT surge in long-lived fly strains abolishes their longevity/proteostasis benefits. The early-life PT elevation triggers proteostatic dysfunction, silences stress responses, and drives age related functional decline via juvenile hormone-lipid transfer protein axis and germline signaling. Our findings suggest that PT is adaptively suppressed after early-adulthood, alleviating later-life proteostatic burden, slowing down age-related functional decline, and improving lifespan. Our work provides a theoretical framework for understanding how lifetime PT dynamics shape future aging trajectories.
2023-10-24 | PXD044118 | Pride
Project description:Aging is associated with fundamental changes in pancreatic B-cell physiology; yet, the mechanisms that drive these age-related changes are poorly understood. We performed comprehensive proteomic profiling of pancreatic islets from adolescent and old mice. The analysis revealed striking differences in abundance of enzymes controlling glucose metabolism not reflected at the transcript level. We show that these changes in protein abundance are associated with increased activity of the amplifying pathway of insulin secretion. The amplifying pathway stimulates insulin secretion through coupling factors produced during glucose metabolism. Nutrient tracing and targeted metabolomics demonstrate accelerated accumulation of glucose-derived metabolites and coupling factors in aged islets, indicating that age-related changes in glucose metabolism contribute to the improved response of B-cells to glucose with age. Together, our study provides the first in-depth characterization of changes in the islet proteome during aging and establishes metabolic rewiring as an important mechanism for age-associated changes in B-cell function.
2017-10-03 | MSV000081577 | MassIVE
Project description:Cellular senescence is a stress response that imposes stable cell-cycle arrest in damaged cells, preventing their propagation in tissues. However, long-term presence of senescent cells might promote tissue degeneration and malignant transformation via secreted pro-inflammatory and matrix-remodeling factors. These factors lead to immune-cell recruitment and senescent-cell clearance. Senescent cells accumulate in tissues in advanced age. The extent of immune-system involvement in regulating age-related accumulation of senescent cells, and its consequences, are unknown. Here we show that mice with impaired cell cytotoxicity exhibit both higher senescent-cell tissue burden and chronic inflammation. They suffer from multiple age-related disorders and significantly lower survival. Strikingly, pharmacological elimination of senescent-cells by ABT-737 partially alleviates accelerated aging phenotype in these mice. In progeroid mice, impaired cell cytotoxicity further promotes senescent-cell accumulation and shortens lifespan. ABT-737 administration during the second half of life of these progeroid mice abrogates senescence signature and increases median survival. Our findings shed new light on mechanisms governing senescent-cell presence in aging, and could motivate new strategies for regenerative medicine.
2018-11-20 | GSE115401 | GEO
Project description:Humans show remarkable variation in susceptibility to infectious diseases as well as chronic inflammatory and autoimmune disorders. This heterogeneity arises partially from variation in the immune response, which is responsible for preventing and controlling infection. To better understand the major factors driving antiviral immune response differences, we used single-cell RNA-sequencing to measure the effects of genetic ancestry and cis-regulatory variation on the transcriptional response to influenza infection in various immune cell types in 90 European and African American individuals. We show that monocytes are the most responsive to infection but that all cell types engage a conserved, type I IFN response, which is stronger in European individuals. Further, we detect directional, polygenic differences in expression phenotypes between populations that are under cis-genetic control and show that recent positive selection has acted on putatively causal risk loci associated with common autoimmune disorders. Our findings establish genetic ancestry and common cis-regulatory variants as important determinants governing the antiviral immune response, thus improving our understanding of the factors that contribute to differences in infectious and complex disease susceptibility.
2021-11-26 | GSE162632 | GEO
Project description:Background: Age is the strongest breast cancer risk factor, with overall breast cancer risk increasing steadily beginning at approximately 30 years of age. However, while breast cancer risk is lower among younger women, young women’s breast cancer may be more aggressive. Though several genomic and epidemiologic studies have shown higher prevalence of aggressive, estrogen-receptor negative breast cancer in younger women, the age-related gene expression that predisposes to these tumors is poorly understood. Characterizing age-related patterns of gene expression in normal breast tissues may provide insights on etiology of distinct breast cancer subtypes that arise from these tissues. Methods: To identify age-related changes in normal breast tissue, 96 tissue specimens from reduction mammoplasty patients aged 14 to 70 were assayed by gene expression microarray. Results: Significant associations between gene expression levels and age were identified for 802 probes (481 increased, 321 decreased with increasing age). Enriched functions included ‘aging of cells’, ‘shape change’, and ‘chemotaxis’, and enriched pathways included Wnt/beta-catenin signaling, Ephrin Receptor Signaling, and JAK/Stat Signaling. Applying the age-associated genes to publicly available tumor datasets, the age-associated pathways defined two groups of tumors with distinct survival. Conclusion: The hazard rates of young-like tumors mirrored that of high grade tumors in the Surveillance, Epidemiology and End Results Program, providing a biological link between normal aging and age-related tumor aggressiveness. Impact: These data show that studies of normal tissue gene expression can yield important insights about the pathways and biological pressures that are relevant during tumor etiology and progression. reference x sample
2013-08-31 | E-GEOD-43973 | biostudies-arrayexpress
Project description:Virus-specific memory T cells generated during primary infection and maintained in tissues and circulation are capable of initiating a quick and robust response upon secondary exposure to viral antigens. To understand the nature of this recall response and the factors that determine antiviral T cell function, we performed single-cell transcriptome profiling of virus-specific CD8+ T cells across diverse tissue sites following stimulation with viral antigens using pooled library amplification for transcriptome expression sequencing (PLATE-seq)(Bush et al., 2017). From this analysis, we found that antigen-responsive cells primarily cluster based on tissue and not virus specificity, with the exception of CMV-specific T cells from the BM. These findings suggest tissue-regulated antiviral T cell function, with specific CMV-driven influences in the BM.
2022-01-05 | GSE178837 | GEO