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Mesenchymal TNFR2 promotes the development of polyarthritis and comorbid heart valve stenosis.

ABSTRACT: Mesenchymal TNFR2 promotes the development of polyarthritis and comorbid heart valve stenosis.

PROVIDER: PRJNA427313 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6412310.fastq.gz	Fastqsanger.gz
	SRR6412320.fastq.gz	Fastqsanger.gz
	SRR6412311.fastq.gz	Fastqsanger.gz
	SRR6412312.fastq.gz	Fastqsanger.gz
	SRR6412303.fastq.gz	Fastqsanger.gz

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Mesenchymal TNFR2 promotes the development of polyarthritis and comorbid heart valve stenosis.

Project description:This study demonstrates that arthritis and heart valve stenosis comorbidity, the most common condition among RA and SpA patients, share common mesenchymal requirements converging in the pathogenic activation of resident mesenchymal origin fibroblasts in the TnfARE mouse model. TNFR2 signaling, in this context, orchestrates the molecular mechanisms underlying arthritis and heart valve stenosis manifestation by regulating fibroblasts pathogenic activation status, cell proliferation and pro-inflammatory milieu. Finally this work highlights the complexity of TNFR2 functions since mesenchymal signaling is detrimental, whereas systemic TNFR2 provides protective signals that contain both pathologies

2018-04-23 | GSE108451 | GEO

Mesenchymal TNFR2 promotes the development of polyarthritis and comorbid heart valve stenosis.

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Project description:BACKGROUND: Calcific aortic valve stenosis (CAVS) is the most prevalent valvular heart disease in developed countries with significant morbidity and mortality. Given the poor understanding of the pathophysiological processes leading to CAVS, we utilized a joint non-targeted metabolomics and targeted lipidomics approach to better characterize the metabolic perturbations involved in its development and progression.METHODS: We collected human aortic valve tissue from 106 patients undergoing aortic valve replacement surgery. Our cohort represented aortic valvular hemodynamics from mild to severe aortic stenosis with varying degrees of valvular calcification.RESULTS: Seventy-two significantly differential (p<0.01) metabolites across different stages of CAVS severity were filtered and identified from the tissue metabolome. Each stage of valvular stenosis was characterized by a distinct metabolic signature. The top three perturbed metabolic pathways in the setting of CAVS involved glycerophospholipid metabolism, linoleic acid metabolism and primary bile acid biosynthesis. The lysophosphatidic acid species (LysoPA) exhibited significant (p<0.05) association with CAVS severity and were also found to select patients with accelerated rate of CAVS progression. Two LysoPA species namely, 18:2 LysoPA and 20:4 LysoPA, exhibited potential to serve as biomarkers of CAVS severity.CONCLUSIONS: The present study reports the largest and most comprehensive metabolomics analysis of human aortic valve stenosis that highlights the dysregulated LysoPA pathway involved in the pathogenesis of CAVS.

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