High salt diet and uveitis
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB65938 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR12036217.fastq.gz | Fastqsanger.gz | |||
| ERR12036218.fastq.gz | Fastqsanger.gz | |||
| ERR12036219.fastq.gz | Fastqsanger.gz | |||
| ERR12036220.fastq.gz | Fastqsanger.gz | |||
| ERR12036221.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 58 |
Similar Datasets
Project description:We report the comparison of low salt vs high salt diet fed Dahl rat kidney glomeruli by sequencing analysis
2023-09-01 | GSE237521 | GEO
Project description:To identify the effect of high-salt diet on immune cells of brain tissues, we isolated immune cells of brain from mice fed with control diet or high-salt diet.
2022-08-24 | GSE199459 | GEO
Project description:we analyzed the influence of a high-salt diet on liver by transcriptome sequencing. We found that after high-salt feeding, many metabolic abnormalities had formed based on transcriptome sequencing results. Analyses of differentially expressed genes revealed that at least 15 enzyme activities and the metabolism of multiple substances were affected by a high-salt diet. Moreover, a variety of signaling, and metabolic pathways, as well as biological functions, including some known pathways and many novel ones, such as retinol metabolism, linoleic acid metabolism, steroid hormone biosynthesis, and signaling pathways, were involved in liver dysfunction due to a high-salt diet.
2020-12-17 | GSE163294 | GEO
Project description:High salt diet-induced functional adaptions in bone marrow progenitor cells, which subsequently reduced monocyte-derived macrophage reparative phenotype and impeded stroke recovery
2023-08-29 | GSE214728 | GEO
Project description:The goal of this study is to understand the effects of high salt diet on metabolic changes in different tissues including liver, WAT and muscle through RNA-seq. Methods: Liver, WAT and muscle mRNA profiles of control WT and 12wks high salt diet fed mice were generated by RNA deep sequencing, using Illumina Hiseq 6000. Sequenced reads were trimmed for adaptor sequence, and masked for low-complexity or low-quality sequence, then mapped to mm10 whole genome using Hisat2. Results: We observed that several genes associated with de novo lipogenesis and cholesterol biosynthesis were significantly down-regulated in WAT and liver tissue of HSD mice group. Besides, combined with secretome datasets, our results further demonstrated that high salt diet could also down-regulate different organokines, and thus, possibly mediate crosstalk between different metabolic tissues Conclusions: Our study investigated the mechanisms of changed gene expression pattern of metabolic organs induced by high salt in terms of whole transcriptome profiling.
2022-03-08 | GSE197972 | GEO
Project description:Diet High in salt content have been associated with cardiovascular disease and chronic inflammation. We recently demonstrated that transient receptor potential canonical 3 (TRPC3) channels regulate myofibroblast transdifferentiation in hypertrophic scars. Here, we examined how high salt activation of TRPC3 participates in hypertrophic scarring during wound healing. In vitro, we confirmed that high salt increased the TRPC3 protein expression and the marker of myofibroblast alpha smooth muscle actin (α-SMA) in wild-type mice (WT) primary cultured dermal fibroblasts but not Trpc3-/- mice. Activation of TRPC3 by high salt elevated cytosolic Ca2+ influx and mitochondrial Ca2+ uptake in dermal fibroblasts in a TRPC3-dependent manner. High salt activation of TRPC3 enhanced mitochondrial respiratory dysfunction and excessive reactive oxygen species (ROS) production by inhibiting pyruvate dehydrogenase action, that activated ROS-triggered Ca2+ influx and the Rho kinase/MLC pathway in WT mice but not Trpc3-/- mice. In vivo, a persistent high-salt diet promoted myofibroblast transdifferentiation and collagen deposition in a TRPC3-dependent manner. Therefore, this study demonstrates that high salt enhances myofibroblast transdifferentiation and promotes hypertrophic scar formation through enhanced mitochondrial Ca2+ homeostasis, which activates the ROS-mediated pMLC/pMYPT1 pathway. TRPC3 deficiency antagonizes high salt diet-induced hypertrophic scarring. TRPC3 may be a novel target for hypertrophic scarring during wound healing.
2023-10-24 | PXD042087 | Pride
Project description:Several studies have established a link between high-salt diet, inflammation, and hypertension. Vitamin D supplementation has shown anti-inflammatory effects in many diseases; gut microbiota is also associated with a wide variety of cardiovascular diseases, but potential role of vitamin D and gut microbiota in high-salt diet-induced hypertension remains unclear. Therefore, we used rats with hypertension induced by a high-salt diet as the research object and analyzed the transcriptome of their tissues (kidney and colon) and gut microbiome to conduct an overall analysis of the gut–kidney axis. We aimed to confirm the effects of high salt and calcitriol on the gut–kidney immune system and the composition of the intestinal flora. We demonstrate that consumption of a high-salt diet results in hypertension and inflammation in the colon and kidney and alteration of gut microbiota composition and function. High-salt diet-induced hypertension was found to be associated with seven microbial taxa and mainly associated with reduced production of the protective short-chain fatty acid butyrate. Calcitriol can reduce colon and kidney inflammation, and there are gene expression changes consistent with restored intestinal barrier function. The protective effect of calcitriol may be mediated indirectly by immunological properties. Additionally, the molecular pathways of the gut microbiota-mediated BP regulation may be related to circadian rhythm signals, which needs to be further investigated. An innovative association analysis of the microbiota may be a key strategy to understanding the association between gene patterns and host.
2021-10-12 | GSE184844 | GEO
Project description:In the present study we made use of the (1-renin) DOCA-salt mouse model - which has been previously shown to develop cardiac and renal hypertrophy - to evaluate the direct effects of high-salt diet on cardiac function and gene expression profiling. The comparison between low-salt and high-salt DOCA-treated mice will reveal what genes are directly modulated by sodium in (normotensive) DOCA-treated mice. Previous publications: Wang Q, Hummler E, Nussberger J, Clement S, Gabbiani G, Brunner HR, Burnier M. Blood pressure, cardiac, and renal responses to salt and deoxycorticosterone acetate in mice: role of renin genes. J Am Soc Nephrol. 2002;13:1509 –1516. Wang Q, Domenighetti AA, Pedrazzini T, Burnier M. Potassium supplementation reduces cardiac and renal hypertrophy independent of blood pressure in DOCA/salt mice. Hypertension. 2005 Sep;46(3):547-54. Keywords: comparative dose-response treatment (2 groups)
2007-01-01 | GSE5946 | GEO
Project description:Transcriptional profiling related cytokines and chemokines of mouse kidneys comparing the kidneys of WNK4 D561A/+ mice fed an 8% high-salt diet with those of WNK4+/+ littermates with a normal diet. Goal was to determine the effects of a high-salt condition on the immune system in kidney.
2017-06-12 | GSE87600 | GEO
Project description:Compositional changes in the microbiota (dysbiosis) may be a basis for Irritable Bowel Syndrome (IBS) but biomarkers are currently unavailable to direct microbiota-directed therapy. We therefore examined whether changes in fecal β-defensin could be a marker of dysbiosis in a murine model. Experimental dysbiosis was induced using four interventions relevant to IBS: a mix of antimicrobials, westernized diets (high-fat/high-sugar and, high salt diets), or mild restraint stress. Fecal mouse β-defensin-3 and 16S rRNA-based microbiome profiles were assessed at baseline, during and following these interventions. Each intervention, except for mild restraint stress, altered compositional and diversity profiles of the microbiota. Exposure to antimicrobials or a high-fat/high-sugar diet, but not mild restraint stress, resulted in decreased fecal β-defensin-3 compared to baseline. In contrast, exposure to the high salt diet increased β-defensin-3 compared to baseline but this was not accompanied by discernible inflammatory changes in the host.
2023-07-11 | GSE225272 | GEO