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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. 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.

ORGANISM(S): Mus musculus

SUBMITTER: Lei Yan

PROVIDER: E-GEOD-26681 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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

Project description:Transcriptional profiling of new born mouse kidney collecting duct (CD) cells comparing the infuence of gestational high salt stress on gene expression remolding of BdkrB2 receptor knockout CD cells with that of BdkrB2 receptor wild type CD cells. 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 collecting duct gene expression pattern. Single color microarray experiment, BdkrB2 knockout new born mouse CD cells vs. BdkrB2 WT mosue CD cells with both on gestational high salt stress. Biological replicates: 3 BdkrB2 null replicates, 3 BdkrB2 WT replicates. Expression level of each sample was normalized to WT1 replicate.

2013-08-08 | E-GEOD-49616 | biostudies-arrayexpress

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.

2011-01-19 | GSE26681 | GEO

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

2013-08-08 | GSE49616 | GEO

Mus musculus

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

| PRJNA136585 | ENA

Urinary phosphate-containing nanoparticle contributes to inflammation and kidney injury in salt-sensitive hypertension

Project description:Although disturbed phosphate metabolism frequently accompanies chronic kidney disease, it is unclear whether it contributes to the progression of renal dysfunction. Here, we show that urinary phosphate-containing nanoparticles promote kidney injury in salt-sensitive hypertension. Remarkably, four weeks of high salt loading resulted in a 2.5-fold increase in urinary phosphate excretion in Dahl salt-sensitive rats on a normal phosphorus diet. Inhibition of intestinal phosphate absorption using sucroferric oxyhydroxide (SF) in this model suppressed phosphaturia, attenuating glomerulosclerosis and tubulointerstitial injury without significantly affecting serum phosphate, blood pressure, or urinary sodium levels. In the kidney, macrophage infiltration and inflammatory cytokine induction were ameliorated by SF. Additionally, macrophage infiltration but not myofibril hypertrophy was alleviated in the heart. In vitro, phosphate loading to proximal tubule cells significantly increased inflammatory cytokine Ccl2, which was abolished by the removal of phosphate-containing nanoparticles but not by the knockdown of phosphate transporter Slc34a1. Finally, transcriptome analysis revealed a potential role of complement C1q in renal inflammation associated with disturbed phosphate metabolism. These data demonstrate that increased phosphaturia promotes inflammation and renal injury from an early stage of salt-sensitive hypertension, and suggest the need for interventions against subclinical phosphate accumulation to improve the prognosis of hypertensive kidney disease.

2020-08-22 | GSE143440 | GEO

Transcriptomic Analysis in Renal T Lymphocytes Exposes Sodium-Independent Dietary Differences in Dahl Salt-Sensitive Rats

Project description:Background. The Dahl salt-sensitive (SS) rat is an established model of salt-sensitive hypertension and renal damage. Recently, sodium-independent dietary effects were shown to be important in the development of the SS hypertensive phenotype. Compared to Dahl SS/JrHsdMcwi (SS/MCW) rats fed a purified diet (AIN-76A), grain-fed Dahl SS/JrHsdMcwiCrl rats (SS/CRL; Teklad 5L2F) were less susceptible to salt-induced hypertension and renal damage. Methods. With the known role of the immune system in hypertension, the present study characterized the immune cells infiltrating SS/MCW and SS/CRL kidneys. To further identify distinct molecular pathways between SS/MCW and SS/CRL, transcriptomic analysis was performed via RNA sequencing in T-cells isolated from the blood and kidneys of low and high salt-fed rats. Results. Following a 3-week high salt (4.0% NaCl) challenge, SS/CRL rats were protected from salt-induced hypertension (116.5±1.2 vs 141.9±14.4 mmHg) and albuminuria (21.7±3.5 vs 162.9±22.2 mg/day) compared to SS/MCW. Additionally, the absolute number of immune cells infiltrating the kidney was significantly reduced in SS/CRL. RNA-seq revealed >50% of all annotated genes in the entire transcriptome to be significantly differentially expressed in T-cells isolated from blood versus kidney. Pathway analysis of significant differentially expressed genes between SS/MCW and SS/CRL renal and circulating T-cells demonstrated salt-induced changes in genes related to inflammation in SS/MCW compared to metabolism-related pathways in SS/CRL. Conclusions. These functional and transcriptomic T-cell differences between SS/MCW and SS/CRL show that sodium-independent dietary effects may influence the immune response and infiltration of immune cells into the kidney, ultimately impacting susceptibility to salt-induced hypertension and renal damage.

2019-08-26 | GSE127000 | GEO

A Parathyroid Hormone/Salt Inducible Kinase Signaling Axis Controls Renal Vitamin D Activation and Organismal Calcium Homeostasis

Project description:The renal actions of parathyroid hormone (PTH) promote 1,25-vitamin D generation; however, the signaling mechanisms in renal epithelial cells downstream of the PTH receptor that control vitamin D metabolism remain unknown. Here we demonstrate that Salt Inducible Kinases (SIKs) control renal 1,25-vit D production downstream of PTH signaling via regulating Cyp27b1 expression. As PTH inhibits the cellular activity of SIKs by cAMP-dependent PKA phosphorylation in bone, we hypothesized that SIKs would also work as an essential mediator of PTH doownstream signaling in kidney, thus regulate vitamin D metabolism. Whole tissue and single cell transcriptomics in kidney demonstrates that both PTH and pharmacologic SIK inhibitors regulate a vitamin D gene module in specific proximal tubule cells. Moreover, small molecule SIK inhibitors directly increase 1,25-vit D production and renal Cyp27b1 mRNA expression in mice and in human embryonic stem cell-derived kidney organoids. Global- and kidney-specific Sik2/Sik3 mutant mice show Cyp27b1 upregulation, elevated serum levels of 1,25-vit D, and PTH-independent hypercalcemia. The SIK substrate CRTC2 shows PTH and SIK inhibitor-inducible binding to key Cyp27b1 regulatory enhancers in the kidney, which are also required for SIK inhibitors to increase Cyp27b1 in vivo. Lastly, in a podocyte injury mouse model of chronic kidney disease (CKD) characterized by low 1,25-vit D levels, SIK inhibitor treatment stimulates both renal Cyp27b1 expression and 1,25-vit D production.

2023-01-01 | GSE207800 | GEO

A Parathyroid Hormone/Salt Inducible Kinase Signaling Axis Controls Renal Vitamin D Activation and Organismal Calcium Homeostasis [SK]

2023-03-01 | GSE207733 | GEO

A Parathyroid Hormone/Salt Inducible Kinase Signaling Axis Controls Renal Vitamin D Activation and Organismal Calcium Homeostasis [SIK]

2023-03-01 | GSE207731 | GEO

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

2020-12-22 | GSE127332 | GEO

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