Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Yin Yang 1 Deficiency in Skeletal Muscle Stem Cell Aggravates Muscle Fibrosis in Duchenne Muscular Dystrophy Mouse by Disrupting Muscle Stem Cell/Macrophage/Fibro-adipogenic Progenitor Crosstalk [ChIP-Seq]

ABSTRACT: Yin Yang 1 Deficiency in Skeletal Muscle Stem Cell Aggravates Muscle Fibrosis in Duchenne Muscular Dystrophy Mouse by Disrupting Muscle Stem Cell/Macrophage/Fibro-adipogenic Progenitor Crosstalk [ChIP-Seq]

PROVIDER: PRJNA1052651 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR27215082_1.fastq.gz	Fastqsanger.gz
	SRR27215082_2.fastq.gz	Fastqsanger.gz
	SRR27215083_1.fastq.gz	Fastqsanger.gz
	SRR27215083_2.fastq.gz	Fastqsanger.gz

Items per page:

1 - 4 of 4

Similar Datasets

Yin Yang 1 Deficiency in Skeletal Muscle Stem Cell Aggravates Muscle Fibrosis in Duchenne Muscular Dystrophy Mouse by Disrupting Muscle Stem Cell/Macrophage/Fibro-adipogenic Progenitor Crosstalk [Hi-C]

Project description:Adult skeletal muscle stem cells (MuSCs), also known as satellite cells (SCs), are widely believed to be responsible for muscle regeneration, which is regulated by complex networks of intrinsic and extrinsic factors. Emerging evidence demonstrates extrinsic regulations from other cell types can significantly impact the regeneration process, especially in repetitive cycles of degeneration/regeneration environment. Here, we demonstrate that the transcription factor (TF) Yin Yang 1 (YY1) deletion in MuSCs of mdx mouse induces CCL5 expression by alleviating the repressive effect on 3D structural interactions on Ccl5 locus. This leads to the increased secretion of CCL5 from MuSCs to the muscle niche, which promotes the recruitment of macrophages (MPs) through the CCL5/CCR5 axis. Incremental MPs lead to continuous inflammation that promotes the survival of Fibro-adipogenic progenitors’ (FAP) through secreting elevated TGFβ1 to stimulate FAPs resisting apoptosis, resulting in aggravated dystrophic pathology manifested by exacerbated fibrosis. Inhibition of CCL5/CCR5 axis by Maraviroc injection effectively mitigates muscle dystrophy and enhances muscle performance in YY1 deletion mdx mouse. Altogether, our findings promote us to conclude that YY1 functions as a 3D structural protein to repress Ccl5 production at the transcriptional level in MuSCs, playing a critical role in orchestrating MuSC/MP/FAP crosstalk through CCL5/CCR5 and TGFβ1 signaling. Intrinsic deletion of YY1 in MuSCs disrupts the cellular interactions and leads to skewed muscle niche with aggravated muscle dystrophy upon chronic injury.

2024-11-27 | GSE250193 | GEO

2024-11-27 | GSE250203 | GEO

2024-11-27 | GSE250202 | GEO

2024-11-27 | GSE250197 | GEO

Yin Yang 1 Deficiency in Skeletal Muscle Stem Cell Aggravates Muscle Fibrosis in Duchenne Muscular Dystrophy Mouse by Disrupting Muscle Stem Cell/Macrophage/Fibro-adipogenic Progenitor Crosstalk

Project description:Yin Yang 1 Deficiency in Skeletal Muscle Stem Cell Aggravates Muscle Fibrosis in Duchenne Muscular Dystrophy Mouse by Disrupting Muscle Stem Cell/Macrophage/Fibro-adipogenic Progenitor Crosstalk

| PRJNA1052660 | ENA

| PRJNA1052654 | ENA

| PRJNA1052662 | ENA

| PRJNA1052661 | ENA

Yin Yang 1 regulates cohesin complex protein SMC3 in mouse hematopoietic stem cells

Project description:Yin Yang 1 (YY1) and Structural Maintenance of Chromosomes 3 (SMC3) are two critical chromatin structural factors that mediate long-distance enhancer-promoter interactions and promote developmentally regulated changes in chromatin architecture in hematopoietic stem/progenitor cells (HSPCs). While YY1 plays critical functions in promoting hematopoietic stem cell (HSC) self-renewal and maintaining HSC quiescence, SMC3 is required for proper myeloid lineage differentiation. However, many questions remain unanswered regarding how YY1 and SMC3 interact with each other and impact hematopoiesis. We found that YY1 physically interacts with SMC3 and co-occupies with SMC3 at a large cohort of promoters genome-wide, and YY1 deficiency deregulates the genetic network governing cell metabolism. YY1 occupies the Smc3 promoter and represses SMC3 expression in HSPCs. YY1 regulates HSC metabolic pathways and maintains proper intracellular reactive oxygen species levels in HSCs, and this regulation is independent of YY1- SMC3 axis. Our results establish a distinct YY1-SMC3 axis and its impact on HSC quiescence and metabolism.

2024-03-11 | GSE261032 | GEO

Yin Yang 1 regulates cohesin complex protein SMC3 in mouse hematopoietic stem cells

Project description:Yin Yang 1 regulates cohesin complex protein SMC3 in mouse hematopoietic stem cells

| PRJNA1000898 | ENA