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Persistent JunB Activation in Fibroblasts Disrupts Stem Cell Niche Interactions Enforcing Skin Aging [RNA-seq]

ABSTRACT: Persistent JunB Activation in Fibroblasts Disrupts Stem Cell Niche Interactions Enforcing Skin Aging [RNA-seq]

PROVIDER: PRJNA746263 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15122156.fastq.gz	Fastqsanger.gz
	SRR15122157.fastq.gz	Fastqsanger.gz
	SRR15122158.fastq.gz	Fastqsanger.gz
	SRR15122159.fastq.gz	Fastqsanger.gz
	SRR15122160.fastq.gz	Fastqsanger.gz

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Persistent JunB Activation in Fibroblasts Disrupts Stem Cell Niche Interactions Enforcing Skin Aging

Project description:Persistent JunB Activation in Fibroblasts Disrupts Stem Cell Niche Interactions Enforcing Skin Aging

| PRJNA746260 | ENA

Persistent JunB Activation in Fibroblasts Disrupts Stem Cell Niche Interactions Enforcing Skin Aging [RNA-seq]

Project description:Fibroblasts residing in the connective tissue of all organs constitute the stem cell niche particularly in connective tissue rich organs like skin. Though the impact of the connective tissue resident fibroblasts on stem cell niches and organ aging is an emerging concept, the underlying mechanisms are largely unresolved. Here, we report a novel mechanism of redox-dependent activation of the transcription factor JunB, which through concomitant upregulation of cyclin dependent kinase inhibitor p16INK4A and repression of IGF-1 dependent cell growth and protein translation initiates the installment of irreversible fibroblast senescence. Fibroblast senescence in turn profoundly disrupts the metabolic and structural niche and its essential interactions with different stem cells thus enforcing depletion of stem cells pools and skin tissue decline. In fact, silencing of JunB in a fibroblast niche-specific knock out mouse - by the reinstatement of IGF-1 and p16 levels - fully restored skin stem cell pools and overall tissue integrity of the skin. We here uncovered a previously unreported role of JunB in the control of the endogenous connective tissue niche and identified promising targets to combat skin aging and associated pathologies.

2021-07-16 | GSE180008 | GEO

Persistent JunB Activation in Fibroblasts Disrupts Stem Cell Niche Interactions Enforcing Skin Aging [ATAC-seq]

Project description:Persistent JunB Activation in Fibroblasts Disrupts Stem Cell Niche Interactions Enforcing Skin Aging [ATAC-seq]

| PRJNA746264 | ENA

Persistent JunB Activation in Fibroblasts Disrupts Stem Cell Niche Interactions Enforcing Skin Aging

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

2021-07-16 | GSE180009 | GEO

Persistent JunB Activation in Fibroblasts Disrupts Stem Cell Niche Interactions Enforcing Skin Aging [ATAC-seq]

Project description:ATAC-seq was performed in control murine dermal fibroblasts (MDF) in the absence and presence of rotenone at a concentration of 250µM for 3 hrs), and in freshly isolated control (Co) and Sod2 cKO MDF.

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JUNB ChIP-seq

Project description:JUNB ChIP-seq

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JunB ChIP of human keratinocytes [ChIP-seq]

Project description:This study is designed to determine the direct target genes of JunB transcription factor in human keratinocytes Mice with epidermal deletion of JunB transcription factor displayed a psoriasis-like inflammation. The relevance of these findings to humans and the mechanisms mediating JunB function are not fully understood. Here, we demonstrate that impaired JunB function via gene silencing or overexpression of a dominant negative mutant increased human keratinocyte cell proliferation but decreased cell barrier function. RNA-seq revealed over 500 genes affected by JunB loss-of-function which included an upregulation of an array of proinflammatory molecules relevant to psoriasis. Among these were TNFa, CCL2, CXCL10, IL6R and SQSTM1, an adaptor protein involved in NF-kB activation. ChIP-Seq and gene reporter analyses showed that JunB directly suppressed SQSTM1 through binding to a consensus AP-1 cis-element located around 2 Kb upstream of SQSTM1-trasncription start site. Similar to JunB loss-of-function, SQSTM1-overexpression induced TNFa, CCL2 and CXCL10. Conversely, NF-kB-inhibition genetically with a mutant IkBa or pharmacologically with PDTC prevented cytokine, but not IL6R, induction by JunB-deficiency. Taken together, our findings indicate that JunB controls epidermal growth, barrier formation and proinflammatory responses through direct and indirect mechanisms, pinpointing SQSTM1 as a key mediator of JunB-suppression of NF-kB-dependent inflammation.

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JUNB ChIP-seq

Project description:Genome-wide mapping of JUNB binding sites in U2OS cell line by ChIP-seq.

2022-09-29 | GSE195991 | GEO

JUNB O-GlcNAcylation-mediated Promoter Accessibility of Metabolic Genes Modulates Distinct Epithelial Lineage in Pulmonary Fibrosis

Project description:Harnessing a 3D patient derived organoid model and multi-omics approach, we provide the first inventory of the connection between metabolic alteration, chromatin accessibility, and transcriptional regulation in IPF aberrant epithelial remodeling. This remodeling is characterized by an increase in chromatin accessibility, particularly at JUNB motif-enriched promoter regions proximal to transcription start sites of metabolic and pro-fibrotic genes. Mechanistically, JUNB undergoes O-linked β-N-acetylglucosamine modification (O-GlcNAcylation), a critical step in modulating pro-fibrotic responses to chronic injury. This modification is pivotal in fostering the emergence of aberrant epithelial basal cells in the alveolar niche, a proposed driver of IPF pathology. Our findings reveal a novel link between metabolic dysregulation and cell fate regulation at the chromatin level in fibrosis, mediated by the O-GlcNAc-JUNB axis.

2024-12-17 | GSE281994 | GEO

JunB control of keratinocyte-mediated inflammation [RNA-seq]

Project description:To determne JunB target gene in human keratincoytes Mice with epidermal deletion of JunB transcription factor displayed a psoriasis-like inflammation. The relevance of these findings to humans and the mechanisms mediating JunB function are not fully understood. Here, we demonstrate that impaired JunB function via gene silencing or overexpression of a dominant negative mutant increased human keratinocyte cell proliferation but decreased cell barrier function. RNA-seq revealed over 500 genes affected by JunB loss-of-function which included an upregulation of an array of proinflammatory molecules relevant to psoriasis. Among these were TNFa, CCL2, CXCL10, IL6R and SQSTM1, an adaptor protein involved in NF-kB activation. ChIP-Seq and gene reporter analyses showed that JunB directly suppressed SQSTM1 through binding to a consensus AP-1 cis-element located around 2 Kb upstream of SQSTM1-trasncription start site. Similar to JunB loss-of-function, SQSTM1-overexpression induced TNFa, CCL2 and CXCL10. Conversely, NF-kB-inhibition genetically with a mutant IkBa or pharmacologically with PDTC prevented cytokine, but not IL6R, induction by JunB-deficiency. Taken together, our findings indicate that JunB controls epidermal growth, barrier formation and proinflammatory responses through direct and indirect mechanisms, pinpointing SQSTM1 as a key mediator of JunB-suppression of NF-kB-dependent inflammation.

2015-10-05 | GSE63079 | GEO

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