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Soluble ST2 induces cardiac contractile dysfunction by repressing mitochondrial electron transport chain genes in cardiomyocytes during fulminant myocarditis

ABSTRACT: Soluble ST2 induces cardiac contractile dysfunction by repressing mitochondrial electron transport chain genes in cardiomyocytes during fulminant myocarditis

PROVIDER: PRJNA1089611 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28389626_1.fastq.gz	Fastqsanger.gz
	SRR28389626_2.fastq.gz	Fastqsanger.gz
	SRR28389627_1.fastq.gz	Fastqsanger.gz
	SRR28389627_2.fastq.gz	Fastqsanger.gz
	SRR28389628_1.fastq.gz	Fastqsanger.gz

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Soluble ST2 induces cardiac contractile dysfunction by repressing mitochondrial electron transport chain genes in cardiomyocytes during fulminant myocarditis

Project description:Fulminant myocarditis (FM) is an acute fatal disease characterised by myocardial inflammation. Our previous study identified soluble growth stimulation- expressed gene 2 (sST2) as a sensitive and specific biomarker for early diagnosis of FM. However, its function in FM remains unclear.In the present study, we observed a marked elevation of sST2 in the plasma and hearts of mice with FM induced by coxsackievirus B3 (CVB3) and explored the main cellular sources of sST2 in FM. Moreover, using recombinant sST2 protein administration and unbiased transcriptomics analyses, we investigated the role and underlying mechanisms of sST2 in FM. Importantly, we found that sST2 has a novel non-classical function in cardiomyocytes, other than acting as an IL-33 decoy receptor. These findings reveal a novel role and action mechanism of sST2 in FM and suggest that sST2 may be a potential therapeutic target for FM.

2024-03-24 | GSE261940 | GEO

Differential expression profiles of plasma tsRNAs in children with fulminant myocarditis

Project description:We report the application of high-throughput RNA sequencing technology to examine expression profiling of plasma transfer RNA (tRNA)-derived small RNAs (tsRNAs) in children with fulminant myocarditis during acute phase (FM-A group), children with fulminant myocarditis during convalescent phase (FM-C group), and healthy volunteers (Con group). A total of 750 precisely matched tsRNAs were identified in the plasma from the three groups. We find that a total of 13 tsRNAs were differentially expressed in FM-A and CON samples, of which 11 tsRNAs were upregulated and 2 were downregulated, and 694 tsRNAs were excluded ; a total of 8 tsRNAs were differentially expressed in paired FM-C and CON samples, of which 2 tsRNAs were upregulated and 6 were downregulated and 703 tsRNAs were excluded . This study provides new ideas for future research on elucidating the mechanisms of myocarditis through regulating tsRNAs levels.

2020-12-29 | GSE163944 | GEO

Plasma exosomal miRNA profiles in pediatric fulminant myocarditis patients and healthy controls

Project description:The pathophysiology of fulminant myocarditis (FM) is significantly influenced by the interactions between immunological and myocardial cells, involving exosome-mediated intercellular microRNA (miRNA) signaling. To further investigate the pathogenesis of FM and discover diagnostic biomarkers, we have employed miRNA microarray expression profiling as a discovery platform.

2023-05-02 | GSE221090 | GEO

Soluble ST2 Is a Sensitive and Specific Biomarker for Fulminant Myocarditis.

Project description:Background The aim of the study was to identify biomarkers that can facilitate early diagnosis and treatment of fulminant myocarditis (FM) in order to reduce mortality. Methods and Results First, the expression profiles of circulating cytokines were determined in the plasma samples from 4 patients with FM and 4 controls using human cytokine arrays. The results showed that 39 cytokines from patients with FM were changed at admission. Among them, 8 cytokines returned to normal levels at discharge, including soluble ST2 (sST2), which showed the most marked dynamic changes from disease onset to resolution. Then, in a cohort of 76 patients with FM, 57 patients with acute hemodynamic dysfunction attributable to other causes, and 56 patients with non-FM, receiver operating characteristic curve analyses suggested that plasma sST2 level was able to differentiate FM from non-FM or other FM-unrelated acute heart failure more robustly N-terminal pro-B-type natriuretic peptide or cardiac troponin I. Moreover, longitudinal analysis of plasma sST2 was performed in 10 patients with FM during hospitalization and 16 patients with FM during follow-up. Finally, the diagnostic value was validated in an additional 26 patients with acute onset of unstable hemodynamics. The cutoff value of plasma sST2 for optimal diagnosis of FM was established at 58.39 ng/mL, where a sensitivity of 85.7% and specificity of 94.7% were achieved. Conclusions Elevated sST2 level was associated with mechanical stress or inflammation. Especially, sST2 might be used as a potential biomarker for the rapid diagnosis of FM, which was characterized by strong mechanical stretch stimulation and severe inflammatory response. Registration URL: https://www.clinicaltrials.gov; Unique identifier: NCT03268642.

| S-EPMC9075487 | biostudies-literature

Serum exosomal miRNA profiles in fulminant myocarditis patients and healthy controls

Project description:Purpose: Exosome-derived microRNAs (miRNAs) are potential diagnostic biomarkers. However, little is known about their effectiveness as diagnostic biomarkers of fulminant myocarditis (FM). This study aimed to explore miRNA levels in serum exosomes of patients with FM as potential biomarkers for FM diagnosis. Methods: 10 samples were screened with a exosomal small RNA sequencing platform (RiboBio). A Mann-Whitney test was performed to discover differentially expressed miRNAs in the two pairwise comparisons: FM versus HC. Results: From the differentially expressed miRNAs, fourteen candidate miRNAs discovered via small RNA sequencing with P＜0.05 and fold expression change ＞2 were selected for further testing Conclusions: These data suggested that the miRNA panel in serum-derived exosomes provided excellent diagnostic capability for FM.

2021-01-27 | GSE147517 | GEO

Serum exosomal miRNA profiles in fulminant myocarditis patients and healthy controls

Project description:Serum exosomal miRNA profiles in fulminant myocarditis patients and healthy controls

| PRJNA615110 | ENA

Differential expression profiles of plasma tsRNAs in children with fulminant myocarditis

Project description:Differential expression profiles of plasma tsRNAs in children with fulminant myocarditis

| PRJNA688297 | ENA

Differential expression profiles and functional analysis of circulating small extracellular vesicle-derived lncRNA in children with fulminant myocarditis

Project description:Fulminant myocarditis (FM) is the most serious type of childhood myocarditis. However, the molecular mechanism underlying the pathogenesis of FM has not been fully elucidated. Studies have shown that small extracellular vesicles (sEVs) play important roles in many diseases, but any potential role of sEVs in pediatric FM has not been reported. Here, the differential expression profiles of lncRNAs in plasma sEVs were studied in five children with FM and five healthy children using whole transcriptome sequencing, followed by functional analysis and screening of immune-related target genes. A total of 68 up-regulated and 11 down-regulated differentially expressed sEVs-lncRNAs were identified. Functional analysis showed that the differentially-expressed sEVs-lncRNAs were mainly involved in immune processes, apoptosis, and protein efflux. Further analysis of immune-related target genes revealed that differentially expressed sEVs-lncRNAs were closely related to immune activation, immune cell migration and cytokine pathway signal transduction in FM. Thus, sEVs-lncRNAs may play an important role in the pathogenesis of FM in children

2023-03-31 | GSE226412 | GEO

Plasma exosomal miRNA profiles in pediatric fulminant myocarditis patients and healthy controls

Project description:Plasma exosomal miRNA profiles in pediatric fulminant myocarditis patients and healthy controls

| PRJNA912731 | ENA

Mast Cells Control Lung Type 2 Inflammation via Prostaglandin E2-Driven Soluble ST2.

Project description:Severe asthma and sinus disease is a consequence of Type 2 inflammation (T2I), mediated by IL-33 signaling through its membrane-bound receptor, ST2. Soluble (s)ST2 reduces available IL-33 and limits T2I, but little is known about its regulation. We demonstrate that prostaglandin E2 (PGE2) drives production of sST2 to limit features of lung T2I. PGE2 deficient mice display diminished sST2. In humans with severe respiratory T2I, urinary PGE2 metabolites correlate with serum sST2. In mice, PGE2 enhanced sST2 secretion by mast cells (MCs). Mice lacking MCs, ST2 expression by MCs or EP2 receptors by MCs showed reduced sST2 lung concentrations and strong T2I. Recombinant sST2 reduced T2I in mice lacking PGE2 or ST2 expression by MCs back to control levels. PGE2 deficiency also reversed the hyperinflammatory phenotype in mice lacking ST2 expression by MCs. PGE2 thus suppresses T2I through MC-derived sST2, explaining the severe T2I observed in low PGE2 states.

2024-05-20 | GSE266501 | GEO

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