Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1105049 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28813207_1.fastq.gz | Fastqsanger.gz | |||
| SRR28813207_2.fastq.gz | Fastqsanger.gz | |||
| SRR28813208_1.fastq.gz | Fastqsanger.gz | |||
| SRR28813208_2.fastq.gz | Fastqsanger.gz | |||
| SRR28813209_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.
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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.
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Project description:Engulfment by macrophages is critical for waste clearance in the vertebrate brain. Understanding clearance mechanisms may open new therapeutic possibilities to counter brain aging and neurodegenerative diseases. However, few in vivo models exist to study engulfment in the brain and characterize this process during aging and across species. Here we present a genetic model for secretion of a fluorescent protein by neurons in the brain of the African turquoise killifish, the shortest-lived vertebrate that can be bred in captivity. We use this model to identify a population of brain macrophages in the killifish responsible for engulfment of material from the brain extracellular space. Intriguingly, many of these cells bear similarities to mammalian border-associated and monocyte-derived macrophages, rare subsets of macrophages in mouse and human brains noted for their engulfment capabilities. We also find that in our model, killifish brain macrophages decline in engulfment capacity with age. This work highlights how vertebrate brain macrophages, particularly those at brain border regions, can play a critical role in clearance and provides an opportunity to test interventions that can boost engulfment by these macrophages to promote brain resilience in old age and disease.
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Project description:A single-cell RNA sequencing dataset of cardiac aging in African Turquoise Killifish
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Project description:Aging individuals exhibit a pervasive decline in adaptive immune function, with important implications for health and lifespan. Previous studies have found a pervasive loss of immune-repertoire diversity in human peripheral blood; however, little is known about repertoire aging in other immune compartments, or in species other than humans. Here, we perform the first study of immune-repertoire aging in an emerging model of vertebrate aging, the African turquoise killifish (Nothobranchius furzeri). Despite their extremely short lifespans, these killifish exhibit complex and individualised heavy-chain repertoires, with a generative process capable of producing millions of distinct productive sequences. Whole-body killifish repertoires decline rapidly in within-individual diversity with age, while between-individual variability increases. Large, expanded B-cell clones exhibit far greater diversity loss with age than small clones, suggesting an important difference in the age-sensitivity of different B cell populations. Compared to the whole body, the immune repertoires of isolated intestinal samples exhibit much more dramatic age-related phenotypes, apparently due to an elevated prevalence of age-sensitive expanded clones. Our results highlight the importance of organ-specific dynamics in adaptive immunosenescence.
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Project description:Aging is a major contributor to functional decline of the heart and various cardiovascular diseases. Alterations across different cardiac cell types must be tightly orchestrated during normative aging process that has begun to be mapped at the transcriptional level through single-cell RNA-sequencing. However, current rodent models are limited in their capacity to experimentally test large numbers of candidate differentially expressed genes (DEGs). As an attractive alternative, the African Turquoise Killifish (ATK) promises more efficient genetic studies of cardiac aging because it has the shortest lifespan among vertebrates. Despite its experimental advantages, single-cell transcriptomic studies on cardiac aging in ATK have not yet been conducted. Here, we generated the first scRNA-seq profiles of hearts from young and old GRZ strain ATK and demonstrated changes in cellular composition, gene expression, functional pathways, and intercellular communication during cardiac aging.
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