The gene expression signatures in young and aging C57BL/6 mouse kidney
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ABSTRACT:
PROVIDER: PRJNA415621 | ENA |
REPOSITORIES: ENA
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Project description:To identify novel aging-related miRNAs, we initially established a physiological aging mouse model (20-month old male C57BL/6 mouse), compared with 2-month old male C57BL/6 mouse. Then, the Agilent miRNA microarray was performed to profile miRNA expression levels in kidney from 20-month old male C57BL/6 mouse (designated as Aging) and 2-month old male C57BL/6 mouse (designated as Young).
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Project description:To monitor the mRNA expression profiling in aging process, we initially established a physiological aging mouse model (20-month old male C57BL/6 mouse), compared with 2-month old male C57BL/6 mouse. Then, the Agilent mRNA microarray was performed to profile the gene expression levels in kidney from 20-month old male C57BL/6 mouse (designated as Aging) and 2-month old male C57BL/6 mouse (designated as Young).
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Project description:The miRNA expression signatures in young and aging C57BL/6 mouse kidney
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Project description:Studies on aging have largely included one or two OMICS layers, which may not necessarily reflect the signatures of other layers. Moreover, most aging studies have often compared very young (4-5 wks) mice with old (24 months) mice which does not reflect the aging transition after the attainment of adulthood. Therefore, we aimed to study and compared muti-OMICS aging signatures across key metabolic tissues of mature adults (6 months) and old (24 months) C57BL/6J mice (the most commonly used mouse strain). Here we compared the differentially regulated genes and enriched pathways for transcriptome, proteome and epigenome (H3K27ac, H3K4me3, H3K27me3, DNA methylation) across liver, heart, and quadriceps muscle. The major aging associated pathways cross multiple layers and tissues are decreased RNA metabolism, transcription, and translation at transcript and protein levels however increased potential of transcription at DNA methylation and H3K27ac levels.
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Project description:Aging is accompanied by a gradual loss of systemic metabolic homeostasis, which is maintained by multiple-organs, especially the kidney and kidney. However, a systematic study of the regulatory networks and regulatory transcription factors (TFs) of aging in the kidney and kidney remains lacking. Here, we performed an integrated analysis of multi-omics datasets in the kidney and kidney from young and aged mice, including RNA-seq, reduced representation bisulfite sequencing (RRBS) and ATAC-seq datasets, which indicated that enhanced inflammation and dysregulated metabolism were conserved signatures in aged kidney and kidney in both the transcriptome and epigenome. Transcription factor and regulatory network analysis indicated that activation of AP-1 and SPI1 was responsible for enhanced inflammation, and down-regulation of HNFs and PPARs contributed to dysregulated metabolism in aged kidney and kidney. Importantly, we found that the activation of AP-1 was cellular autonomous in aged hepatic and renal cells. However, enhanced SPI1 was caused by elevated infiltration of macrophages. Importantly, inhibition of AP-1 with small molecule combination attenuated inflammation phenotypes of aging in vivo and in vitro. Taken together, our analysis revealed common signatures and regulatory TFs of aging in the kidney and kidney, providing novel targets for the development of anti-aging interventions.
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Project description:The kidney governs many physiological factors of the body, and the glomerulus is its core filtration unit. Glomeruli comprise of less than 1.5% of the kidney’s volume and thus are underrepresented in many analyses of the kidney, and require particular isolation methods. Aging is a major risk factor for kidney disease, yet despite the importance of proper glomerular function, we have limited knowledge of the changes that glomerular cells undergo during aging. Here we interrogate the aged mouse kidney, glomerulus and glomerular cells using various approaches, including single cell RNA sequencing (scRNA-Seq), to identify age and senescence associated changes at the tissue and cellular level. We show that the aged kidney and glomerulus undergo structural changes, including increased fibrosis, glomerulonephritis and expression of injury and senescence-associated markers. Lastly, we utilized our method for high-throughput analysis of mouse glomeruli to characterize cell-specific and age-related changes in glomerular cells. This analysis revealed a senescence-associated phenotype in aged mesangial cells, and emphasized the potential importance of mesangial cells and macrophages in this niche. Our study provides insights into the molecular and cellular changes of the aging glomerulus that suggest therapeutic targets for age-related renal dysfunction.
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