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Gestational high salt stressed Embryonic Day 14.5 BdkrB2 Null Mouse Kidney vs. BdkrB2 Wild Type Mouse Kidney

ABSTRACT: Transcriptional profiling of Embryonic Day 14.5 mouse kidneys comparing the infuence of gestational high salt stress on gene expression remolding of BdkrB2 receptor null mice with that of BdkrB2 receptor wild type mice. The BdkrB2 receptor has been shown to be playing a role in renal vascular tone, kidney secretion and reabsorption function, normal kidney development, while impaired BdkrB2 receptor in kidney shown being associated with renal agenesis and renal dysplasia. Goal was to determine the effects of BdkrB2 receptor knockout together with gestational high salt stress on renal gene expression pattern.

ORGANISM(S): Mus musculus

PROVIDER: GSE26681 | GEO | 2011/01/19

SECONDARY ACCESSION(S): PRJNA136585

REPOSITORIES: GEO

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Gestational high salt stressed Embryonic Day 14.5 BdkrB2 Null Mouse Kidney vs. BdkrB2 Wild Type Mouse Kidney

Project description:Transcriptional profiling of Embryonic Day 14.5 mouse kidneys comparing the infuence of gestational high salt stress on gene expression remolding of BdkrB2 receptor null mice with that of BdkrB2 receptor wild type mice. The BdkrB2 receptor has been shown to be playing a role in renal vascular tone, kidney secretion and reabsorption function, normal kidney development, while impaired BdkrB2 receptor in kidney shown being associated with renal agenesis and renal dysplasia. Goal was to determine the effects of BdkrB2 receptor knockout together with gestational high salt stress on renal gene expression pattern. Two-condition experiment, BdkrB2 null mouse kidney vs. BdkrB2 WT mosue kidney with both on gestational high salt stress . Biological replicates: 3 BdkrB2 null/WT replicates, 3 BdkrB2 WT/null replicates, all 6 replicates were duplicated.

2011-01-19 | E-GEOD-26681 | biostudies-arrayexpress

Gestational high salt stressed new born BdkrB2 knockout collecting duct cells vs BdkrB2 wild type collecting duct cells

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Gene Expression of Kidney from HSRA-S (congenital solitary kidney) and HSRA-C (two-kidney) using Rat Gene 1.1 ST Array [RaGene-1_1-st]

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Gene Expression of Kidney from HSRA-S (congenital solitary kidney) and HSRA-C (two-kidney) using Rat Gene 1.1 ST Array [RaGene-1_1-st]

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ERRγ coordinates a transcriptional program of mitochondrial and renal reabsorptive functions implicated in kidney disease [ChIP-seq]

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Global analysis of kidney gene expression by RNA-Seq of aged CTRP1-deficient mice

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

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2019-06-24 | PXD010032 | Pride

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