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Disruption of the Uty epigenetic regulator locus in hematopoietic cells phenocopies the profibrotic attributes of Y chromosome loss in heart failure

ABSTRACT: Disruption of the Uty epigenetic regulator locus in hematopoietic cells phenocopies the profibrotic attributes of Y chromosome loss in heart failure

PROVIDER: PRJNA1008262 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25732308_1.fastq.gz	Fastqsanger.gz
	SRR25732308_2.fastq.gz	Fastqsanger.gz
	SRR25732309_1.fastq.gz	Fastqsanger.gz
	SRR25732309_2.fastq.gz	Fastqsanger.gz
	SRR25732310_1.fastq.gz	Fastqsanger.gz

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Disruption of the Uty epigenetic regulator locus in hematopoietic cells phenocopies the profibrotic attributes of Y chromosome loss in heart failure

Project description:Heart failure is a prevalent condition that affects millions of people worldwide with men exhibiting a higher incidence than women. However, the mechanisms underlying this sex difference remain poorly understood. Our previous work has shown that the presence of mosaic loss of Y chromosome (LOY) in leukocytes is causally associated with increased risk for heart failure. In the current study, we show that LOY macrophages from the failing hearts of humans with dilated cardiomyopathy exhibit widespread changes in gene expression that correlate with fibroblast activation in the myocardium, and we identify the ubiquitously transcribed tetratricopeptide Y linked (Uty) gene in leukocytes as a causal locus for accelerated progression of heart failure in male mice with LOY. Using single-cell multiomics analysis, we demonstrate that Uty disruption leads to epigenetic alterations in both monocytes and macrophages, increasing the propensity of differentiation into pro-fibrotic macrophages that can contribute to cardiac fibrosis and dysfunction. These findings shed light on the mechanisms that contribute to the higher incidence of heart failure in males and suggest potential targets for treatment of heart failure patients with LOY in leukocytes.

2024-01-22 | GSE241486 | GEO

Disruption of the <i>Uty</i> epigenetic regulator locus in hematopoietic cells phenocopies the profibrotic attributes of Y chromosome loss in heart failure.

Project description: Not available

| S-EPMC11343478 | biostudies-literature

Integrin beta-1 (Itgb1) in profibrotic myofibroblasts

Project description:Fibrosis due to extracellular matrix (ECM) secretion from myofibroblasts complicates many chronic liver diseases causing scarring and organ failure. Integrin-dependent interaction with scar ECM promotes profibrotic features. This microarray study was performed to clarify the role of integrin beta-1 (Itgb1) in profibrotic myofibroblasts.

2016-08-18 | E-MTAB-4810 | biostudies-arrayexpress

have identical attributes

Project description:have identical attributes Transcriptome or Gene expression

| PRJNA999054 | ENA

Functional redundancy between UTY and UTX in regulating the localization of transcription factors involved in pluripotency [ATAC-seq]

Project description:The Y chromosome retains a limited number of protein-coding genes, yet their biological significance remains poorly understood. Here, we find UTY, a Y-linked homolog of the histone demethylase UTX, plays an essential regulator of pluripotency in human embryonic stem cells. Despite its low expression and weak enzymatic activity, UTY co-localizes with UTX at active cis-regulatory elements and contributes to the regulation of core pluripotency genes such as NODAL and LEFTY. Through genome-wide occupancy and transcriptome analyses of knockout cell lines, we show that UTY and UTX function redundantly to maintain proper localization of key transcription factors including OCT4 and SOX2. Dual loss of UTY and UTX leads to their mislocalization, widespread transcriptional dysregulation, and loss of pluripotency, without changes in H3K27 methylation. Instead, these effects are associated with changes in histone acetylation and altered chromatin accessibility, likely driven by recruitment of ATP-dependent chromatin remodelers, pointing to a non-enzymatic mechanism. Our findings uncover a novel role for UTY in stabilizing transcription factor binding and maintaining cell identity, demonstrating that even the evolutionarily compact Y chromosome retains critical regulatory functions in early human development.

2026-04-09 | GSE301296 | GEO

Functional redundancy between UTY and UTX in regulating the localization of transcription factors involved in pluripotency [ChIP-seq_dualcross]

2026-04-09 | GSE301295 | GEO

Functional redundancy between UTY and UTX in regulating the localization of transcription factors involved in pluripotency [ChIP-seq]

2026-04-09 | GSE301294 | GEO

Functional redundancy between UTY and UTX in regulating the localization of transcription factors involved in pluripotency [RNA-seq]

2026-04-09 | GSE301297 | GEO

Effects of a Uty gene trap on the transcriptomic profile of mouse cardiac left ventricles in response to castration

Project description:Previous results from the laboratory showed that the genetic make up of chromosome Y modulated the effects of castration on the transcriptome of mouse cardiac left ventricles. To test the effect of the chromosome Y Uty locus, the current study tests how castration affects the transcriptomes of cardiac left ventricles from adult male carrying a Uty gene trap (KO) in comparison to wild-type (WT)couterparts.

2021-09-19 | GSE158370 | GEO

Y chromosome linked UTY modulates sex differences in valvular fibroblast methylation in response to nanoscale extracellular matrix cues

Project description:Aortic valve stenosis (AVS) is a progressive disease wherein males develop valve calcification relative to females that develop valve fibrosis. Valvular interstitial cells (VICs) aberrantly activate to myofibroblasts during AVS, driving the fibrotic valve phenotype in females. Myofibroblasts further differentiate into osteoblast-like cells and secrete calcium nanoparticles, driving valve calcification in males. We hypothesized the lysine demethylase UTY (ubiquitously transcribed tetratricopeptide repeat containing, Y-linked) decreases methylation uniquely in response to nanoparticle cues in the valve extracellular matrix to promote an osteoblast-like phenotype. Here, we describe a bioinspired hydrogel cell culture platform to interrogate how nanoscale cues modulate sex-specific methylation states in VICs activating to myofibroblasts and osteoblast-like cells. We found UTY (ubiquitously transcribed tetratricopeptide repeat containing, Y-linked) modulates VIC phenotypes in response to nanoscale cues uniquely in males. Overall, we reveal a novel role of UTY in the regulation of calcification processes in males during AVS progression.

2024-12-09 | GSE273612 | GEO

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