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Atf3 controls transitioning in female mitochondrial cardiomyopathy as identified by single-cell transcriptomics [snRNA-seq]

ABSTRACT: Atf3 controls transitioning in female mitochondrial cardiomyopathy as identified by single-cell transcriptomics [snRNA-seq]

PROVIDER: PRJNA1014957 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25996146_1.fastq.gz	Fastqsanger.gz
	SRR25996146_2.fastq.gz	Fastqsanger.gz
	SRR25996147_1.fastq.gz	Fastqsanger.gz
	SRR25996147_2.fastq.gz	Fastqsanger.gz
	SRR25996148_1.fastq.gz	Fastqsanger.gz

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Atf3 controls transitioning in female mitochondrial cardiomyopathy as identified by single-cell transcriptomics [snRNA-seq]

Project description:Oxidative phosphorylation defects results in mitochondrial diseases, with cardiac involvement markedly impacting prognosis. However, the mechanisms underlying the transition from compensation to dysfunction in response to metabolic deficiency remain unclear, impeding the development of effective treatments. Here, we employed single-nucleus RNA sequencing (snRNA-seq) on hearts from mitochondrial cardiomyopathy (MCM) mice with cardiac-specific Ndufs6 knockdown of (FS6KD). Pseudotime trajectory analysis of cardiomyocytes from early stage of female FS6KD hearts revealed dynamic cellular state transitioning from compensation to severe compromise, coincided with transient upregulation of a critical transcription factor, activating transcription factor 3 (Atf3). Genetic ablation or adeno-associated virus-mediated Atf3 knockdown in FS6KD mice effectively delayed cardiomyopathy progression in a female-specific manner. Notably, human MCM snRNA-seq revealed a similar transition, including the dynamic expression of ATF3. In conclusion, our findings highlight a fate-determining role of Atf3 in female MCM progression, providing a promising therapeutic candidate for the currently intractable disease.

2025-04-03 | GSE242820 | GEO

Atf3 controls transitioning in female mitochondrial cardiomyopathy as identified by single-cell transcriptomics [PIC_RNA-seq]

2025-04-03 | GSE242818 | GEO

Atf3 controls transitioning in female mitochondrial cardiomyopathy as identified by single-cell transcriptomics [Spatial Transcriptomics]

2025-04-03 | GSE282635 | GEO

Atf3 controls transitioning in female mitochondrial cardiomyopathy as identified by single-cell transcriptomics [RNA-seq]

2025-04-03 | GSE242819 | GEO

Atf3 controls transitioning in female mitochondrial cardiomyopathy as identified by single-cell transcriptomics

Project description:Atf3 controls transitioning in female mitochondrial cardiomyopathy as identified by single-cell transcriptomics

| PRJNA1014902 | ENA

Atf3 controls transitioning in female mitochondrial cardiomyopathy as identified by single-cell transcriptomics [Spatial Transcriptomics]

Project description:Atf3 controls transitioning in female mitochondrial cardiomyopathy as identified by single-cell transcriptomics [Spatial Transcriptomics]

| PRJNA1189511 | ENA

Atf3 controls transitioning in female mitochondrial cardiomyopathy as identified by single-cell transcriptomics [PIC_RNA-seq]

Project description:Atf3 controls transitioning in female mitochondrial cardiomyopathy as identified by single-cell transcriptomics [PIC_RNA-seq]

| PRJNA1014897 | ENA

Atf3 controls transitioning in female mitochondrial cardiomyopathy as identified by single-cell transcriptomics [RNA-seq]

Project description:Atf3 controls transitioning in female mitochondrial cardiomyopathy as identified by single-cell transcriptomics [RNA-seq]

| PRJNA1014956 | ENA

Atf3 controls transitioning in female mitochondrial cardiomyopathy as identified by single-cell transcriptomics

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

2025-04-03 | GSE242821 | GEO

ATF3 is a novel regulator of mouse neutrophil migration.

Project description:Expression of the activating transcription factor 3 (ATF3) gene is induced by Toll-like receptor (TLR) signaling. In turn, ATF3 protein inhibits the expression of various TLR-driven pro-inflammatory genes. Given its counter-regulatory role in diverse innate immune responses, we defined the effects of ATF3 on neutrophilic airway inflammation in mice. ATF3 deletion was associated with increased lipopolysaccharide (LPS)-driven airway epithelia production of CXCL1, but not CXCL2, findings concordant with a consensus ATF3-binding site identified solely in the Cxcl1 promoter. Unexpectedly, ATF3-deficient mice did not exhibit increased airway neutrophilia after LPS challenge. Bone marrow chimeras revealed a specific reduction in ATF3-/- neutrophil recruitment to wild type lungs. In vitro, ATF3-/- neutrophils exhibited a profound chemotaxis defect. Global gene expression analysis identified ablated Tiam2 expression in ATF3-/- neutrophils. TIAM2 regulates cellular motility by activating Rac1-mediated focal adhesion disassembly. Notably, ATF3-/- and ATF3-sufficient TIAM2 knockdown neutrophils, both lacking TIAM2, exhibited increased focal complex area, along with excessive CD11b-mediated F-actin polymerization. Together, our data describe a dichotomous role for ATF3-mediated regulation of neutrophilic responses: inhibition of neutrophil chemokine production, but promotion of neutrophil chemotaxis. Ly6G+ neutrophils were purified by magnetic beads from WT or ATF3 KO bone marrow and RNA was immediately isolated for global gene expression using microarrays.

2014-04-05 | E-GEOD-53973 | biostudies-arrayexpress

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