Mild dehydration effects on the murine kidney single nucleus transcriptome and chromatin accessibility
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA973115 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24601500.fastq.gz | Fastqsanger.gz | |||
| SRR24601501.fastq.gz | Fastqsanger.gz | |||
| SRR24601502.fastq.gz | Fastqsanger.gz | |||
| SRR24601503.fastq.gz | Fastqsanger.gz | |||
| SRR24601504_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 48 |
Similar Datasets
Project description:The kidney is composed of > 40 cell types that work collectively to maintain fluid-electrolyte balance. If not enough fluid is consumed to remain in balance, then vasopressin is released and acts in the kidney to increase water reabsorption. Here the authors used kidney single nucleus multiome-sequencing to determine cell-specific transcriptomes and chromatin accessibility profiles of male and female control (ad libitum water and food) or mildly dehydrated mice (ad libitum food, water deprivation). There were hundreds of sex- and dehydration-specific differentially expressed genes throughout the kidney, most of which did not have a significant change in chromatin accessibility. Thus, even mild dehydration causes cell- and sex-specific transcriptomic changes even though the kidney function to conserve water is the same.
2023-10-13 | GSE232662 | GEO
Project description:The kidney is composed of > 40 cell types that work collectively to maintain fluid-electrolyte balance. If not enough fluid is consumed to remain in balance, then vasopressin is released and acts in the kidney to increase water reabsorption. Here the authors used kidney single nucleus multiome-sequencing to determine cell-specific transcriptomes and chromatin accessibility profiles of male and female control (ad libitum water and food) or mildly dehydrated mice (ad libitum food, water deprivation). There were hundreds of sex- and dehydration-specific differentially expressed genes throughout the kidney, most of which did not have a significant change in chromatin accessibility. Thus, even mild dehydration causes cell- and sex-specific transcriptomic changes even though the kidney function to conserve water is the same.
2023-10-13 | GSE232792 | GEO
Project description:Mild dehydration effects on the murine kidney single nucleus transcriptome and chromatin accessibility [RNA-seq]
| PRJNA973969 | ENA
Project description:Microarray experiment with polysomal and non-polysomal RNAs extracted under non-stress and mild-dehydration stress.
2008-06-12 | E-GEOD-2268 | biostudies-arrayexpress
Project description:Goal of the study was to compare single cell (sc) and single nucleus (sn) sequencing of murine kidney after mild (17min) and severe (27min) ischemia reperfusion injury
2022-04-26 | GSE193649 | GEO
Project description:The hypothalamo-neurohypophyseal system (HNS) is crucial for osmoregulation. The HNS consists of the magnocellular neurons (MCNs) of the hypothalamus that have their axons terminating in the posterior pituitary. The HNS exerts its role in water balance via the release of the anti-diuretic hormone vasopressin (VP). Following dehydration VP is released into the general circulation. By binding to V2-type receptors located in the kidney, VP decrease the amount of water lost in urine. An osmotic stimulus also elicits an increase in VP gene expression and a functional remodelling of the entire HNS. We want to understand this plasticity in terms of the co-ordinated reprogramming of gene expression. We thus used Affymetrix U34a rat GeneChips to examine the dynamics of gene expression plasticity over the duration of a dehydration stimulus. Arrays were probed in triplicate with targets derived from SON of control rats, and rats dehydrated for 1 and for 3 days. Transcripts were thus identified that respond early to dehydration (up- or down-regulated after only 1day of dehydration), or that respond late (up- or down-regulated at 3 days of dehydration). Keywords: SON, Dehydration, clone
2006-08-15 | GSE3131 | GEO
Project description:The kidney is a major organ in which fluid balance and waste excretion is regulated. To obtain mature functions of the kidney, normal renal developmental processes need to be preceded. Comprehensive genetic programs underlying renal development during prenatal life have been widely studied. However, postnatal renal development, from infancy to juvenile period, have not been studied yet. Here, we investigated if structural and functional kidney development was still undergoing in early life by analyzing renal transcriptional networks of infant (4 weeks old) and juvenile (7 weeks old) mice. We further examined the effects of dehydration on kidney development. Kidneys at 4 weeks and 7 weeks old showed significantly distinctive functional network of genes. Gene sets related to cell cycle regulators and immature glomerular barrier integrity (COL4A1, COL4A2) were enriched in infantile kidneys while genes associated with ion transport and drug metabolism (CYP450 family) were shown in juvenile kidneys. Dehydration during infancy suppressed renal growth by interrupting SHH signaling pathway which targets cell cycle regulators. Importantly, disruption of developmental program ultimately led to long-term alterations in renal filtration function, by causing a decline in glomerular filtration barrier integrity. Taken together, we provide meaningful perspectives of renal development in infancy which suggests molecular and physiological background why infants are more vulnerable to dehydration than adults. These results provide new insights into the systemic effects of dehydration on renal development and may propose possible markers for clinical application in pediatric dehydration.
2016-07-01 | GSE75604 | GEO
Project description:The magnocellular neurons (MCNs) of the supraoptic nucleus (SON) and paraventricular nucleus (PVN) of the hypothalamus are the principal site of biosynthesis of prepropeptide precursor of the antidiuretic hormone vasopressin (VP). This precursor is processed during anterograde axonal transportation to terminals in the posterior pituitary gland, where biologically active VP is stored until released into the general circulation in response to physiological activation of the SON by osmotic cues. By binding to V2-type receptors located in the kidney, VP decreases the amount of water lost in urine. Osmotic activation of the SON is accompanied by a dramatic morphological and functional remodelling. We have sought to understand the mechanistic basis of this plasticity in terms of the differential expression of genes. To identify such genes, we adopted an unbiased global approach based on Suppressive Subtractive Hybridisation-Polymerase Chain Reaction (SSH-PCR) Using this method, we generated libraries of clones putatively differentially expressed in control vs dehydrated SON. In order to rapidly screen these libraries, 1152 clones were subjected to microarray analysis, resulting in the identification of 459 differentially expressed transcripts. cDNA clones corresponding 56 of these RNAs were sequenced, revealing many of them to be novel ESTs. Four transcripts were shown by in situ hybridisation (ISH) to be significantly up- or down-regulated in the SON following dehydration. These genes may represent novel effectors or mediators of SON physiological remodelling. Keywords: dehydration, SON, NIA
2005-12-02 | GSE3133 | GEO
Project description:Single nucleus inDrops to profile adult human kidney
2018-06-19 | GSE114156 | GEO
Project description:Background- CINAC-patients can be identified by the recently discovered renal proximal tubular cell lysosomal lesions which are also observed in patients experiencing calcineurin inhibitor (CNI) nephrotoxicity, suggesting that CINAC is a toxin-induced nephropathy. An alternative hypothesis advocates chronic heat stress/dehydration as the major etiological factor for CINAC. Here, we evaluated in rats to what extent heat stress/dehydration reflects the renal CINAC histopathology in humans. Methods- Wistar rats were divided in 3 groups. Group 1(n=6) had free access to drinking water (control group). Group 2(n=8) was water deprived for 10 hours per 24hr, 5 days/week and placed in an incubator (37°C) for 30 min/hr during water deprivation. Group 3(n=8) underwent daily oral gavage with cyclosporine (40mg/kg body weight). After 28 days kidneys were collected for light- and electron microscopic histopathology and proteomic analysis. Results- Cyclosporine rats developed renal cortical lesions mimicking those of CINAC patients i.e. atrophic proximal tubules with associated tubulo-interstitial fibrosis. PASM staining demonstrated enlarged argyrophilic granules in the affected proximal tubules, identified as lysosomes by LAMP1 immunofluorescent staining. Electron microscopy confirmed the presence of enlarged dysmorphic lysosomes, closely mimicking the dysmorphic lysosomes seen in CINAC-patients. Dehydration was demonstrated by urinary osmolality and fluctuating body weight but showed none of the histological features of CINAC patients. Proteomic analysis confirmed cellular toxicity of cyclosporine, whereas the dehydration group lacked any of these toxicity markers. Conclusion- Dehydration/heat stress alone does not lead to the renal proximal tubular and interstitial lesions as observed in CINAC-patients. The histopathological analogy between CINAC and CNI nephrotoxicity in rats and humans and CINAC supports the toxicological etiology.
2022-11-14 | PXD038062 | Pride