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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

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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:Gut microbial metabolite trimethylamine N-oxide aggravates pulmonary hypertension

| PRJNA786337 | ENA

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

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.

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Aging, Dementia, and TBI Study

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Project description:Gene expression profiling was performed on frontal and temporal cortex from vascular dementia (VaD), Alzheimer's disease (AD), and non-demented controls (Control) obtained from the University of Michigan Brain Bank. Controls and AD cases had no infarcts in the autopsied hemisphere. Vascular dementia cases had low Braak staging.

2019-04-23 | GSE122063 | GEO

Methylation arrays (MethylationEPIC) of peripheral blood of individuals with evolving dementia

Project description:DNA methylation changes have been associated to dementia and cognitive decline. However, it is not clear if these changes arise before or during the onset of the pathologies. Here, using Illumina's MethylationEPIC array technology, we have profiled the methylomes of elderly, cognitively healthy individuals which go on to develop dementia or stay cognitively healthy. The subjects are profiled at a pre-diagnosis stage and at 4 year follow-up post-diagnosis.

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Identification of the binding DNA of ONECUT2 by ChIP in Neuro-2a cells

Project description:These ChIP-seq analyses identified binding DNAs of ONEUCT2 in Neuro-2a (mouse neuroblastoma)cells. We overexpressed OC2ΔHOX (a gain-of-function mutant) in Neuro-2a cells, and infected the cells with HSV-1 at 40 hours post transfection. Samples infected for 5 hours were sequenced by ChIP for binding DNAs of the OC2 mutant in Neuro-2a cells.

2023-09-18 | GSE241863 | GEO

Time-dependent specific molecular signatures of inflammation and remodelling are associated with Trimethylamine-N-oxide (TMAO)-induced endothelial cell dysfunction

Project description:Cardiovascular diseases (CVDs) are leading causes of death worldwide. Endothelial dysfunction is a critical initiating factor contributing to CVDs, which progression involves the gut microbiome-derived metabolite Trimethylamine N-oxide (TMAO). Here, we aim to clarify the time-dependent pathways by which TMAO mediates endothelial dysfunction.

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