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IRF3 and type I interferons fuel a fatal response to myocardial infarction

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE106473 | GEO | 2017/11/06

SECONDARY ACCESSION(S): PRJNA416978

REPOSITORIES: GEO

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IRF3 and type I interferons fuel a fatal response to myocardial infarction.

Project description:Interferon regulatory factor 3 (IRF3) and type I interferons (IFNs) protect against infections and cancer, but excessive IRF3 activation and type I IFN production cause autoinflammatory conditions such as Aicardi-Goutières syndrome and STING-associated vasculopathy of infancy (SAVI). Myocardial infarction (MI) elicits inflammation, but the dominant molecular drivers of MI-associated inflammation remain unclear. Here we show that ischemic cell death and uptake of cell debris by macrophages in the heart fuel a fatal response to MI by activating IRF3 and type I IFN production. In mice, single-cell RNA-seq analysis of 4,215 leukocytes isolated from infarcted and non-infarcted hearts showed that MI provokes activation of an IRF3-interferon axis in a distinct population of interferon-inducible cells (IFNICs) that were classified as cardiac macrophages. Mice genetically deficient in cyclic GMP-AMP synthase (cGAS), its adaptor STING, IRF3, or the type I IFN receptor IFNAR exhibited impaired interferon-stimulated gene (ISG) expression and, in the case of mice deficient in IRF3 or IFNAR, improved survival after MI as compared to controls. Interruption of IRF3-dependent signaling resulted in decreased cardiac expression of inflammatory cytokines and chemokines and decreased inflammatory cell infiltration of the heart, as well as in attenuated ventricular dilation and improved cardiac function. Similarly, treatment of mice with an IFNAR-neutralizing antibody after MI ablated the interferon response and improved left ventricular dysfunction and survival. These results identify IRF3 and the type I IFN response as a potential therapeutic target for post-MI cardioprotection.

| S-EPMC6477926 | biostudies-literature

IRF3 and type I interferons fuel a fatal response to myocardial infarction [bulk RNA-Seq]

Project description:Interferon regulatory factor 3 (IRF3) and type I interferons (IFNs) protect against infections1 and cancer2, but excessive IRF3 activation and type I IFN production cause autoinflammatory conditions such as Aicardi?Goutières syndrome3,4 and STING-associated vasculopathy of infancy (SAVI)3. Myocardial infarction (MI) elicits inflammation5, but the dominant molecular drivers of MI-associated inflammation remain unclear. Here we show that ischemic cell death and uptake of cell debris by macrophages in the heart fuel a fatal response to MI by activating IRF3 and type I IFN production. In mice, single-cell RNA-seq analysis of 4,215 leukocytes isolated from infarcted and non-infarcted hearts showed that MI provokes activation of an IRF3?interferon axis in a distinct population of interferon-inducible cells (IFNICs) that were classified as cardiac macrophages. Mice genetically deficient in cyclic GMP-AMP synthase (cGAS), its adaptor STING, IRF3, or the type I IFN receptor IFNAR exhibited impaired interferon-stimulated gene (ISG) expression and, in the case of mice deficient in IRF3 or IFNAR, improved survival after MI as compared to controls. Interruption of IRF3-dependent signaling resulted in decreased cardiac expression of inflammatory cytokines and chemokines and decreased inflammatory cell infiltration of the heart, as well as in attenuated ventricular dilation and improved cardiac function. Similarly, treatment of mice with an IFNAR-neutralizing antibody after MI ablated the interferon response and improved left ventricular dysfunction and survival. These results identify IRF3 and the type I IFN response as a potential therapeutic target for post-MI cardioprotection.

2017-11-06 | GSE106471 | GEO

IRF3 and type I interferons fuel a fatal response to myocardial infarction [single cell RNA-Seq]

2017-11-06 | GSE106472 | GEO

IRF3 and type I interferons fuel a fatal response to myocardial infarction

Project description:IRF3 and type I interferons fuel a fatal response to myocardial infarction

| PRJNA416978 | ENA

IRF3 and type I interferons fuel a fatal response to myocardial infarction [bulk RNA-Seq]

Project description:IRF3 and type I interferons fuel a fatal response to myocardial infarction [bulk RNA-Seq]

| PRJNA417168 | ENA

IRF3 and type I interferons fuel a fatal response to myocardial infarction [single cell RNA-Seq]

Project description:IRF3 and type I interferons fuel a fatal response to myocardial infarction [single cell RNA-Seq]

| PRJNA417199 | ENA

miRNA expression data from the hearts of myocardial infarction model

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-01-07 | E-GEOD-76604 | biostudies-arrayexpress

Identification of Novel Serum Biomarkers for Early Decision of ST-elevation Myocardial Infarction

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-05-23 | E-GEOD-61145 | biostudies-arrayexpress

Sex differences in neutrophil biology modulate response to type I Interferons and immunometabolism

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-06-29 | GSE145231 | GEO

Myocardial Infarction accelerates breast cancer via innate immune reprogramming

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-06-11 | GSE137790 | GEO

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