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Rattus norvegicus

ABSTRACT: IGF-1 gene therapy in aging rats modulates hippocampal genes relevant to memory function

PROVIDER: PRJNA390522 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5683090.fastq.gz	Fastqsanger.gz
	SRR5683083.fastq.gz	Fastqsanger.gz
	SRR5683084.fastq.gz	Fastqsanger.gz
	SRR5683085.fastq.gz	Fastqsanger.gz
	SRR5683086.fastq.gz	Fastqsanger.gz

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IGF-1 gene therapy in aging rats modulates hippocampal genes relevant to memory function

Project description:In rats, learning and memory performance decline during normal aging, which makes this rodent species a suitable model to evaluate therapeutic strategies. In aging rats, insulin-like growth factor-I (IGF-I), is known to significantly improve spatial memory accuracy as compared to control counterparts. A constellation of gene expression changes underlie the hippocampal phenotype of aging but no studies on the effects of IGF-I on the hippocampal transcriptome of old rodents have been documented. Here, we assessed the effects of IGF-I gene therapy on spatial memory performance in old female rats and compared them with changes in the hippocampal transcriptome.

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Transcription profiling of Rattus norvegicus hippocampus cells under prenatal stress

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Caloric restriction reprograms the single-cell transcriptional landscape of Rattus norvegicus aging

Project description:Aging causes a functional decline in tissues throughout the body that may be delayed by caloric restriction (CR). However, the cellular profiles and signatures of aging, as well as those ameliorated by CR, remain unclear. Here, we built comprehensive single-cell and single-nucleus transcriptomic atlases across various rat tissues undergoing aging and CR. CR attenuated aging-related changes in cell type composition, gene expression, and core transcriptional regulatory networks. Immune cells were increased during aging, and CR favorably reversed the aging-disturbed immune ecosystem. Computational prediction revealed that the abnormal cell-cell communication patterns observed during aging, including the excessive proinflammatory ligand-receptor interplay, were reversed by CR. Our work provides multi-tissue single-cell transcriptional landscapes associated with aging and CR in a mammal, enhances our understanding of the robustness of CR as a geroprotective intervention, and uncovers how metabolic intervention can act upon the immune system to modify the process of aging.

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