Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Trimethylamine N-oxide Aggravates Neuro-inflammation via lncRNA Fendrr/miR-145-5p/PXN axis in Vascular Dementia Rats

ABSTRACT: Trimethylamine N-oxide Aggravates Neuro-inflammation via lncRNA Fendrr/miR-145-5p/PXN axis in Vascular Dementia Rats

PROVIDER: PRJNA1051060 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR27175483_1.fastq.gz	Fastqsanger.gz
	SRR27175483_2.fastq.gz	Fastqsanger.gz
	SRR27175484_1.fastq.gz	Fastqsanger.gz
	SRR27175484_2.fastq.gz	Fastqsanger.gz
	SRR27175485_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

Trimethylamine N-oxide Aggravates Neuro-inflammation via lncRNA Fendrr/miR-145-5p/PXN axis in Vascular Dementia Rats

Project description:Vascular dementia (2VO) is the second-most cause of dementia, and our previous investigation showed that Trimethylamine-N-oxide (TMAO) exacerbates cognitive dysfunction and neuropathological changes in 2VO rats. Therefore, this study is aimed to evaluate the mechanism of TMAO in 2VO. Bilateral common carotid artery (2VO) model was established in rats and TMAO (120 mg/kg) was administered for 8 consecutive weeks, 4 weeks preoperatively and 4 weeks postoperatively. High-throughput sequencing was performed to find out the effects of TMAO treatment on lncRNA expression in rat hippocampus and bioinformatics analysis was conducted to identify potential downstream targets. Learning and spatial memory capacities were measured, as well as inflammatory factors. Nissl staining was used to observe neuronal injury in the CA1 area of the hippocampus. TMAO administration upregulated lncRNA Fendrr expression in the rat hippocampus, while the damaging effects of TMAO were counteracted after knockdown of Fendrr. Fendrr was highly expressed in 2VO rats and sponged miR-145-5p, which targets PXN. Silencing of Fendrr or PXN, or promotion of miR-145-5p improved neurological function injury, reduced neuronal damage, as well as repressed inflammation response. Inhibition of miR-145-5p abrogated up Fendrr knockdown mediated influence on 2VO rats. Taken together, our results showed that TMAO inhibits the miR-145-5p/PXN axis by increasing the Fendrr expression, thus exacerbating the development of 2VO.

2024-10-30 | GSE249873 | GEO

Gut microbial metabolite trimethylamine N-oxide aggravates pulmonary hypertension

Project description:Trimethylamine N-oxide (TMAO), a metabolite derived from intestine microbial flora, enhances vascular inflammation in a variety of cardiovascular disease, and the bacterial communities associated with trimethylamine N-oxide (TMAO) metabolism is higher in pulmonary hypertension (PH) patients. The effects of TMAO on PH, however, has not been elucidated. In the present study, we found that circulating TMAO is elevated in intermediate to high-risk PH patients when compared to healthy control or low-risk PH patients. In monocrotaline-induced rat PH models, circulating TMAO is elevated; and reduction of TMAO using 3,3-dimethyl-1-butanol (DMB) significantly decreased right ventricle systolic pressure, pulmonary vascular muscularization in both monocrotaline-induced rat PH and hypoxia induced mice PH models. RNA sequencing of rat lungs on DMB revealed significant suppression of pathways involved in cytokine-cytokine receptor interaction, and cytokine and chemokine signaling. Protein-protein interaction analysis of the differentially expressed transcripts regulated by DMB showed 5 hub genes with a strong connectivity of proinflammatory cytokines and chemokines including Kng1, Cxcl1, Cxcl2, CxcL6 and Il6. In vivo, TMAO significantly increased the expression of Kng1, Cxcl1, Cxcl2, CxcL6 and Il6 in bone marrow derived macrophage. And TMAO-treated conditioned medium from macrophage increased the proliferation and migration of pulmonary artery smooth muscle cells; but TMAO treatment did not change the proliferation or migration of pulmonary artery smooth muscle cells. In conclusion, our study demonstrates that TMAO is increased in severe PH, and the reduction of TMAO using DMB reduces pulmonary vascular muscularization and alleviates PH via suppressing the macrophage production of chemokines and cytokines.

2022-06-07 | GSE190203 | GEO

Single Nuclei Sequencing of old and young mice hearts under senolytica (Ageing impairs the neuro-vascular interface in the heart)

Project description:Aging is a major risk factor for impaired cardiovascular health. The aging myocardium is characterized by microcirculatory and diastolic dysfunction and increased susceptibility to arrhythmias. Nerves align with vessels during development. However, the impact of aging on the cardiac neuro-vascular interface is entirely unknown. Here, we report that aging reduces nerve density specifically in the left ventricle and dysregulates vascular-derived neuro-regulatory genes. Aging leads to a down-regulation of miR-145 and de-repression of the neuro-repulsive factor Semaphorin-3A. miR-145 deletion, which increased Sema3a expression, or endothelial Sema3a overexpression reduced axon density, thus mimicking the observed aged heart phenotype. Removal of senescent cells, which accumulated with chronological age in parallel to the decline in nerve density, rescued age-induced denervation, reduced Sema3a expression, preserved heart rate variability and reduced electrical instability. These data suggest that senescence-associated regulation of neuro-regulatory genes is associated with reduced nerve density and, thereby, contributes to age-associated cardiac dysfunction.

2023-07-05 | E-MTAB-13093 | biostudies-arrayexpress

Gut microbial metabolite trimethylamine N-oxide aggravates pulmonary hypertension

Project description:Gut microbial metabolite trimethylamine N-oxide aggravates pulmonary hypertension

| PRJNA786337 | ENA

Identification of miR-145 targets using SILAC

Project description:miR-145 is downregulated in multiple cancers. The introduction of miR-145 could alleviate the tumor burden in the pancreatic cancer mouse model. However, how miR-145 mediates the tumor suppression is still an open question. In this study, we aimed to identify the targets of miR-145 using a SILAC approach.

2014-10-28 | PXD001260 | Pride

Transcription profiling of Methanosarcina mazei grown with trimethylamine or methanol to investigate the expression pattern of methyltransferase genes

Project description:The genomic expression patterns of Methansarcina mazei growing with trimethylamine or methanol were measured.

2009-08-05 | E-MEXP-2108 | biostudies-arrayexpress

miRNAs regulation by miR-145 in pancreatic cancer

Project description:miR-145 is a tumor suppressor miRNA in various malignancies including pancreatic cancer. How miR-145 regulates expression of other miRNAs could provide a panoramic view of the development of pancreatic cancer. Therefore, in this project, we aimed to characterize how other miRNAs are affected by miR-145 in hope for understanding proteomic changes that are not explained by miR-145 alone.

2013-03-19 | GSE45246 | GEO

Sinorhizobium meliloti strain:145

Project description:Sinorhizobium meliloti 145 Resequencing

| PRJNA501469 | ENA

Gene expression regulation by miR-145 in pancreatic cancer

Project description:miR-145 is a tumor suppressor miRNA in various malignancies including pancreatic cancer. Identification of miR-145 targets can lead to more understanding of the development of pancreatic cancer. Therefore, in this project, we aimed to characterize the changes of transcriptomes caused by miR-145 to identify more miR-145 target transcripts.

2013-03-19 | GSE45245 | GEO

Bradyrhizobium diazoefficiens strain:USDA 145 | isolate:USDA 145

Project description:Bradyrhizobium diazoefficiens USDA 145 genome sequencing

| PRJNA1115750 | ENA