Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1106410 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28844185_1.fastq.gz | Fastqsanger.gz | |||
| SRR28844185_2.fastq.gz | Fastqsanger.gz | |||
| SRR28844186_1.fastq.gz | Fastqsanger.gz | |||
| SRR28844186_2.fastq.gz | Fastqsanger.gz | |||
| SRR28844187_1.fastq.gz | Fastqsanger.gz |
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Project description:In this work we took 9 samples from brain and 6 samples from muscle of the African turquoise killifish (Nothobranchius furzeri) at 3.5, 8.5 and 14 weeks. Total RNA was sequenced and circRNAs were detected.
2019-07-31 | GSE134065 | GEO
Project description:With advancing age, senescent cells accumulate as they are not efficiently cleared by the immune system anymore. Via a senescence-associated secretory phenotype, chronic senescent cells alter the microenvironment, creating an unfavorable milieu for neurogenesis and neurorepair. Using an innovative and rapid aging model, the African turquoise killifish, we have previously demonstrated a dramatic decline in neurogenic potential of non-glial progenitors with age. Even after traumatic brain injury, progenitor proliferation and neuron production was very low in aged killifish in comparison to young adult killifish, and overall neurorepair was incomplete. In the present study, we validated if the senolytic cocktail dasatinib and quercetin (D+Q) could reboot the neurogenic output by clearing chronic senescent cells from the aged killifish brain to re-create the necessary supportive environment. Our results confirm that the aged killifish telencephalon holds a very high senescent cell burden, which we could diminish by short-term systemic D+Q treatment. As a consequence of D+Q administration, proliferation of non-glial progenitors increased and more new neurons were generated and migrated into the parenchyma after injury. Injury-induced inflammation and glial scarring, a phenomenon only seen in aged killifish, remained unaltered. Senolytic treatment with D+Q might thus hold promise for improving brain function in aged populations, and is especially interesting for reviving the neurogenic potential of an already aged central nervous system.
2023-07-20 | PXD036437 | Pride
Project description:Protein aggregation is a hallmark of age-related neurodegeneration. Yet whether aggregation drives age-related dysfunction and disease in other tissues is poorly understood. Here, we leverage the African turquoise killifish to obtain a systematic understanding of protein aggregation in seven tissues in an aging vertebrate.
2020-10-17 | MSV000086315 | MassIVE
Project description:The African turquoise killifish combines a short lifespan with age-dependent loss of neuroregenerative capacity, making it a well-suited model for studying brain repair mechanisms in the context of aging. To investigate the extent of cellular diversity that shapes neuro- and gliogenesis, we performed single cell sequencing of the adult telencephalon. Our analysis identifies seventeen cell types including neuronal cells, and progenitors of glial and non-glial nature. Further subclustering unveils four radial glia (RG) types, one atypical non-glial progenitor (NGP) and two intermediate subtypes. Validation of our data in situ reveals a distinct spatial setting for defined RG subtypes, reflecting the distribution of morphologically and physiologically distinct populations. Lineage inference analysis suggests neuroepithelial-like radial glia and NGP to be the start point and intercessor of neural development, respectively. Neuronal sub-clustering uncovers immature and mature excitatory or inhibitory sub-clusters. This complete catalogue of killifish telencephalon cell types is accessible via an online tool, providing a resource to understand neurogenesis in healthy brains and upon injury or disease.
2024-09-03 | GSE213154 | GEO
Project description:Introduction: Aging is associated with progressive loss of renal function and vascular structure, with and without chronic kidney disease. However, the mechanisms driving renal vascular aging and potential therapeutic interventions remain poorly understood. Methods: To model this state-of-affairs, we used African turquoise killifish (Nothobranchius furzeri), a naturally short-lived vertebrate. We then inhibited the sodium-glucose co-transporter 2 inhibition (SGLT2i) to test a potential therapeutic intervention. Histological, immunofluorescent, and 3D vascular imaging were used to evaluate glomerular, tubular, and vascular changes. Single-nuclei transcriptomic profiling was performed on whole kidneys to identify age- and treatment-associated molecular signatures. Results: Aged killifish kidneys exhibited hallmark features of human renal aging, including glomerulosclerosis, tubular fibrosis, and vascular rarefaction. Functional changes included increased proteinuria and altered tubular transporter expression. Transcriptomic profiling revealed a metabolic shift from oxidative phosphorylation to glycolysis and upregulation of pro-inflammatory pathways. Aged vasculature also displayed a marked reduction in tight junctions and cell–cell contacts. Dapagliflozin attenuated age-related vascular rarefaction, preserved functional peritubular capillary networks, and reduced albuminuria by restoring a youthful transcriptional profile and enhancing intercellular signaling. However, fish lifespan was not extended. Conclusion: This study establishes the killifish as a translational model for investigating renal vascular aging. We show that SGLT2i preserves renal microvascular structure and function, reduces proteinuria, and reprograms the aged transcriptome. These results support a vascular-protective role of SGLT2i in mitigating age-related renal deterioration.
2025-07-30 | GSE297623 | GEO