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Unknown,Transcriptomics,Genomics,Proteomics

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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

SUBMITTER: Lei Yan

PROVIDER: E-GEOD-49616 | 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.

2013-08-08 | GSE49616 | GEO

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 Embryonic Day 14.5 BdkrB2 Null Mouse Kidney vs. BdkrB2 Wild Type Mouse Kidney

2011-01-19 | GSE26681 | GEO

Collecting Duct-Specific Inactivation of HNF-1β Leads to Fibrocystic Disease and Impaired Urinary Concentration

Project description:Hepatocyte nuclear factor-1β (HNF-1β) is an essential transcription factor that regulates tissue-specific gene expression in the kidney, liver, pancreas and genitourinary tract. In humans, mutations of HNF-1β cause renal cysts and diabetes (RCAD) and congenital anomalies of the kidney and urinary tract (CAKUT). Inactivation of Hnf-1β in tubular epithelial cells throughout the nephron leads to early-onset cyst formation and postnatal lethality. Here, we used Pkhd1/Cre mice to delete Hnf-1β specifically in renal collecting ducts (CD). Hnf-1β mutant mice survived long-term and developed slowly progressive cystic kidney disease, renal fibrosis, and hydronephrosis. Compared with wild-type littermates, Hnf-1β mutant mice had higher urine volume, lower urine osmolality, and higher water intake. Differences were seen at baseline, following 24h water restriction, and following administration of dDAVP. Circulating ADH levels were similar in wild type and mutant mice. Polyuria, polydipsia, and decreased urine osmolality were present prior to the onset of cyst formation and hydronephrosis. These findings indicated that Hnf-1β mutant mice have a primary defect in urinary concentrating ability. Studies using in vitro hypertonicity response experiments identified NR1H4 (FXR), a transcription factor previously shown to regulate water homeostasis, as a novel HNF-1β target. mIMCD3 cells exposed to hypertonic medium robustly upregulated Fxr mRNA levels; this upregulation was lost in Hnf-1β mutant cells. HNF-1β was bound to the Fxr promoter region in vivo, and Fxr mRNA was significantly downregulated in mutant mice. FXR protein localized to CD in wild-type mice and was almost undetectable in the cyst epithelium of mutant mice. These findings highlight a new and critical role for HNF-1β in urinary concentration and hypertonicity by regulating the transcription of FXR in the CD.

2017-06-13 | GSE85976 | GEO

Gene expression analysis of collecting duct carcinoma

Project description:We performed a transcriptomic analysis in a cohort of 6 Collecting Duct Carcinoma, 5 Clear Cell Renal Cell Carcinoma and 4 non-matched normal renal tissues to unravel the underlying biological and molecular determinants and to identifiy specific genes and pathways of this rare tumor type.

2021-07-13 | GSE153965 | GEO

Human iPSC-derived renal collecting duct organoids model cystogenesis in ADPKD

Project description:We established the expansion culture of human iPSC-derived ureteric bud tip cells (UBTCs), an embryonic precursor that give rise to collecting ducts (CDs), and succeeded in advancing the developmental stage of CD organoids. We used single cell RNA-sequencing (scRNA-seq) to dissect cell types in CD organoids.

2023-11-29 | GSE237528 | GEO

Osmolality as a major regulator of the transcriptome and metabolome in kidney collecting duct cells

Project description:We hypothesized that altered extracellular osmolality per se could affect the transcriptome of the kidney inner medullary collecting duct (IMCD) cells, and hence it might change renal tubular function. The data sets of transcriptomics were incorporated into the "omic" data sets of metabolomics. Primary cultured IMCD cells of rat kidney were grown in hyperosmolar culture medium (640 mOsm/KgH2O) for 4 d, and then the cells were cultured in the medium with either reduced (300 mOsm/KgH2O) or the same osmolality for 1 or 2 d more.

2012-02-09 | GSE35598 | GEO

Glucocorticoid receptor maintains vasopressin responses in kidney collecting duct cells

Project description:Glucocorticoid receptor maintains vasopressin responses in kidney collecting duct cells

| PRJNA798899 | ENA

Glucocorticoid receptor maintains vasopressin responses in kidney collecting duct cells

Project description:Water permeability of the kidney collecting ducts is regulated in part by the amount of the molecular water channel protein aquaporin-2 (AQP2), whose expression, in turn, is regulated by the pituitary peptide hormone vasopressin. We previously showed that stable glucocorticoid receptor knockdown diminished the vasopressin-induced Aqp2 gene expression in the collecting duct cell model mpkCCD. Here, we investigated the pathways regulated by the glucocorticoid receptor by comparing transcriptomes of the mpkCCD cells with or without stable glucocorticoid receptor knockdown. Glucocorticoid receptor knockdown downregulated 5,394 transcripts associated with 55 KEGG pathways including “vasopressin-regulated water reabsorption,” indicative of positive regulatory roles of these pathways in the vasopressin-induced Aqp2 gene expression. Quantitative RT-PCR confirmed the downregulation of the vasopressin V2 receptor transcript upon glucocorticoid receptor knockdown. Glucocorticoid receptor knockdown upregulated 3,785 transcripts associated with 42 KEGG pathways including the “TNF signaling pathway” and “TGFβ signaling pathway,” suggesting the negative regulatory roles of these pathways in the vasopressin-induced Aqp2 gene expression. Quantitative RT-PCR confirmed the upregulation of TNF and TGFβ receptor transcripts upon glucocorticoid receptor knockdown. TNF or TGFβ inhibitor alone, in the absence of vasopressin, did not induce Aqp2 gene transcription. However, TNF or TGFβ blunted the vasopressin-induced Aqp2 gene expression. In particular, TGFβ reduced vasopressin-induced increases in Akt phosphorylation without inducing epithelial-to-mesenchymal transition or interfering with vasopressin-induced apical AQP2 trafficking. In summary, our RNA-seq transcriptomic comparison revealed positive and negative regulatory pathways maintained by the glucocorticoid receptor for the vasopressin-induced Aqp2 gene expression.

2022-05-16 | GSE194044 | GEO

Aberrant centrosome biogenesis disrupts nephron and collecting duct progenitor growth and fate resulting in fibrocystic kidney disease

Project description:Mutations that disrupt centrosome biogenesis or function cause congenital kidney developmental defects and fibrocystic pathologies. Yet, how centrosome dysfunction results in the kidney disease phenotypes remains unknown. Here, we examined the consequences of conditional knockout of the ciliopathy gene Cep120, essential for centrosome duplication, in the nephron and collecting duct progenitor niches of the mouse embryonic kidney. Cep120 loss led to reduced abundance of both cap mesenchyme and ureteric bud populations, due to a combination of delayed mitosis, increased apoptosis, and premature differentiation of progenitor cells. These defects resulted in dysplastic kidneys at birth, which rapidly formed cysts, displayed increased interstitial fibrosis, and decline in kidney function. RNA sequencing of embryonic and postnatal kidneys from Cep120-null mice identified changes in pathways essential for development, fibrosis, and cystogenesis. Our study defines the cellular and developmental defects caused by centrosome dysfunction during kidney morphogenesis, and identifies new therapeutic targets for patients with renal centrosomopathies.

2023-12-08 | GSE249693 | GEO

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