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Single cell-RNA sequencing for Immune cells from mouse brain post high-salt diet

ABSTRACT: single cell-RNA sequencing for Immune cells from mouse brain post high-salt diet

PROVIDER: PRJNA820023 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18487723.fastq.gz	Fastqsanger.gz
	SRR18487724.fastq.gz	Fastqsanger.gz

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single cell-RNA sequencing for Immune cells from mouse brain post high-salt diet

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.

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Transcriptome sequencing reveals high-salt diet-induced abnormal liver metabolic pathways in mice

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.

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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.

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High-salt diet promotes hypertrophic scarring through TRPC3-mediated mitochondrial Ca2+ homeostasis dysfunction

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.

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2018-09-12 | ST001051 | MetabolomicsWorkbench

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