Global analysis of kidney gene expression by RNA-Seq of aged CTRP1-deficient mice
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ABSTRACT:
PROVIDER: PRJNA524700 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8645710_1.fastq.gz | Fastqsanger.gz | |||
| SRR8645710_2.fastq.gz | Fastqsanger.gz | |||
| SRR8645711_1.fastq.gz | Fastqsanger.gz | |||
| SRR8645711_2.fastq.gz | Fastqsanger.gz | |||
| SRR8645712_1.fastq.gz | Fastqsanger.gz |
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Project description:Aging affects multi-organ systems. What local and systemic factors influence renal structure and function in aging are not well understood. We and others have shown that the secretory protein, C1q/TNF-related protein 1 (CTRP1), regulates systemic metabolism and cardiovascular function. Whether CTRP1 has a role in kidney function is unknown. We provide evidence here that CTRP1 modulates renal physiology in an age- and sex-dependent manner. In addition to adipose tissue, CTRP1 is also expressed in kidney glomeruli, with podocyte being a major cell source. In mice lacking CTRP1, we observed significant increase in kidney weight and glomeruli hypertrophy in aged (~1 year) male, but not female or younger mice. Although glomerular filtration rate, plasma renin and aldosterone levels, and renal response to water restriction are not different between genotypes, aged CTRP1-deficient male mice have elevated blood pressure. Echocardiogram and pulse wave velocity measurements indicate normal heart function and vascular stiffness in CTRP1 knockout animals. Increased blood pressure is not due to greater salt retention. Paradoxically, CTRP1-deficient mice have elevated urinary sodium and potassium excretion, resulting, in part, from reduced expression of genes involved in renal sodium and potassium reabsorption. Despite renal hypertrophy, gene expression related to inflammation, fibrosis, and oxidative stress are significantly lower in CTRP1-deficient mice. RNA sequencing and pathway analyses reveal additional alterations and enrichments of genes in metabolic processes in the kidney of CTRP1-null animals. These results highlight novel contributions of CTRP1 to aging-associated changes in renal structure and function
2020-12-22 | GSE127332 | GEO
Project description:Global analysis of kidney gene expression by RNA-Seq of aged CTRP1-deficient mice on high-fat diet
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Project description:Global transcriptomic changes in aged mouse kidney podocytes
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Project description:Clca1 expression in the aged kidney in mice
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Project description:Like many cell types, the mechanisms and pathways underlying healthy aged-related changes to podocytes are not fully understood. Candidate pathways include oxidative stress, epigenetic changes, senescence, sirtuins, reduced autophagy and increased apoptosis, although detailed mechanisms underlying each pathway is not well defined. While detailed gene analysis has been undertaken on whole portions of the aging kidney, transcriptomic changes specific to podocytes in the aged kidney are not known. To address this, we used an inducible podocyte specific reporter mouse in which a cohort of podocytes are permanently labeled over the life time of the animal. RNA-seq was then used to measure transcriptional changes in genes in labeled podocytes in mice with advanced age, compared to podocytes from a cohort of young reporter mice.
2020-08-20 | GSE136138 | GEO
Project description:Aging and obesity profoundly influence organ system health by altering circulating levels of hormones, growth factors, and cytokines. C1q/TNF-related protein 1 (CTRP1) is an endocrine factor with important metabolic, cardiovascular, and renal functions. We sought to determine the impact of CTRP1 deficiency on heart and kidney function in the context of aging and obesity using aged and obese wild-type (WT) and Ctrp1 knockout (KO) mice fed a high-fat diet for eight months or longer. Surprisingly, no differences were observed in blood pressure, heart function, or vascular stiffness between genotypes. Loss of CTRP1, however, resulted in renal enlargement (relative to body weight), reduced urinary creatinine, elevated urinary total protein content and pH, and changes in renal gene expression affecting sugar, fat, and amino acid metabolism pathways. Assessment of glomerular integrity, the extent of podocyte foot process effacement, as well as renal response to water restriction and salt loading did not reveal significant differences between WT and Ctrp1-KO mice. Interestingly, blood platelet, white blood cell, neutrophil, lymphocyte, and eosinophil counts were significantly elevated, whereas mean corpuscular volume and hemoglobin were reduced in Ctrp1-KO mice. Cytokine profiling revealed increased circulating levels of CCL17 and TIMP-1 in KO mice. Compared to a previous study, our current data suggest that chronic high-fat feeding affects renal phenotypes differently than similarly aged mice fed a control low-fat diet, highlighting a diet-dependent contribution of CTRP1 deficiency to age-related changes in renal structure and function.
2020-10-13 | GSE151154 | GEO
Project description:We compared the complete mouse liver, spleen, lung and kidney transcriptome of adult 13- and 130-wk old wt C57Bl/6J mice (n=3) to develop gene sets for young adult and aged wt mice, respectively
2008-06-01 | E-MEXP-1504 | biostudies-arrayexpress
Project description:In this study, a discovery approach was designed to identify novel mRNA transcripts that may be involved in kidney aging. RNA-Seq revealed increase in the expression of Clca1 mRNA in the aged kidney. CLCA1 facilitates Cl- current operated by TMEM16A, a Ca++-dependent Cl- channel. Cl- movement accompanied by cations such as Na+ and K+ or in exchange for other anions occurs among fluid compartments in many segments of the nephron. Cl- shift among these compartments is governed by electrochemical potential and transporters and exchangers.
2021-06-01 | GSE155407 | GEO
Project description:Mice deficient in the glucocorticoid-regenerating enzyme 11β-HSD1 resist age-related spatial memory impairment. To investigate the mechanisms/pathways involved, we used microarrays to identify differentially expressed hippocampal genes that associate with cognitive ageing and 11β-HSD1. Aged wild-type mice were separated into memory-impaired and unimpaired relative to young controls according to their performance in the Y-maze. All individual aged 11β-HSD1-deficient mice showed intact spatial memory. The majority of differentially expressed hippocampal genes were increased with ageing (e.g. immune/inflammatory response genes) with no genotype differences. However, the neuronal-specific transcription factor, Npas4 and immediate early gene, Arc were reduced (relative to young) in the hippocampus of memory-impaired but not unimpaired aged wild-type or aged 11β-HSD1-deficient mice. Quantitative RT-PCR and in situ hybridization confirmed reduced Npas4 and Arc mRNA expression in memory-impaired aged wild-type mice. These findings suggest that 11β-HSD1 may contribute to the decline in Npas4 and Arc mRNA levels associated with memory impairment during ageing, and that decreased activity of synaptic plasticity pathways involving Npas4 and Arc may, in part, underlie the memory deficits seen in cognitively-impaired aged wild-type mice. 20 samples, 5 groups of 4 biological replicates each. Young, Wild Type animals are overall controls
2015-11-23 | E-GEOD-68515 | biostudies-arrayexpress
Project description:The aging brain shows changes in microglial function, morphology, and phenotype, indicating chronic microglial activation. CX3CR1 is crucial for microglial chemotaxis, phagocytosis, and activation. However, its exact role in the aging brain is not well understood. In this study, we examined the expression of CX3CR1 in the brains of middle-aged mice (10 months old) and explored its functional implications by conducting proteomic profiling in CX3CR1-deficient mouse cerebrum. Proteomic analysis revealed an enrichment of differentially expressed proteins (DE-proteins) in the cerebrum of middle-aged mice in GO pathways such as “synapse”, “translation”, and “ribosome”. CX3CR1 deficiency affected protein levels in GO pathways such as “glutamatergic synapse” and “RNA splicing.” We also detected the proteomics in age-matched 5xFAD mice for comparison, since this mouse strain featured aberrant microglial activation and CX3CR1 upregulation in the hippocampus and frontal cortex. Our findings demonstrated that CX3CR1 was upregulated to maintain synaptic homeostasis probably through regulating microglial activation and phagocytosis in the brains of middle-aged mice. CX3CR1 may represent a promising therapeutic target for alleviating the effects of aging and preventing neurodegeneration.
2025-07-05 | PXD058961 | Pride