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JunB defines functional and structural integrity of the epidermo-pilosebaceous unit in the skin

ABSTRACT: Here we identified JunB, a member of the AP-1 transcription factor family, regulated epidermal stem cells and sebaceous glands through balancing proliferation and differentiation of progenitors and by suppressing lineage infidelity.

ORGANISM(S): Mus musculus

PROVIDER: GSE113688 | GEO | 2018/04/26

REPOSITORIES: GEO

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JunB defines functional and structural integrity of the epidermo-pilosebaceous unit in the skin.

Project description:Transcription factors ensure skin homeostasis via tight regulation of distinct resident stem cells. Here we report that JunB, a member of the AP-1 transcription factor family, regulates epidermal stem cells and sebaceous glands through balancing proliferation and differentiation of progenitors and by suppressing lineage infidelity. JunB deficiency in basal progenitors results in a dermatitis-like syndrome resembling seborrheic dermatitis harboring structurally and functionally impaired sebaceous glands with a globally altered lipid profile. A fate switch occurs in a subset of JunB deficient epidermal progenitors during wound healing resulting in de novo formation of sebaceous glands. Dysregulated Notch signaling is identified to be causal for this phenotype. In fact, pharmacological inhibition of Notch signaling can efficiently restore the lineage drift, impaired epidermal differentiation and disrupted barrier function in JunB conditional knockout mice. These findings define an unprecedented role for JunB in epidermal-pilosebaceous stem cell homeostasis and its pathology.

| S-EPMC6109099 | biostudies-literature

JunB defines functional and structural integrity of the epidermo-pilosebaceous unit in the skin

Project description:JunB defines functional and structural integrity of the epidermo-pilosebaceous unit in the skin

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Lipid metabolizing enzymes differ between preputial gland sebocytes and sebaceous gland sebocytes

Project description:Due to limited model systems for sebaceous glands we investigated potential suitability of preputial glands as model for sebaceous glands. We performed single-cell sequencing of murine preputial glands and back skin biopsies. This study revealed striking differences in lipid metabolizing enzyme expression and differentiation pathways found in sebocytes of the different tissues.

2022-01-24 | GSE185268 | GEO

Small proline-rich proteins 1 and 2 function as antimicrobial proteins in the skin

Project description:Using RNA-sequencing we tested how human sebaceous glands cells respond to bacterial stimuli by comparing the mRNA profiles of sebaceous gland cells treated with lipopolysaccharide to vehicle treated sebaceous gland cells.

2022-03-15 | GSE182756 | GEO

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.

2015-10-05 | GSE63080 | GEO

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 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

Global miRNA expression profiling of Junb-deficient murine embryonic fibroblasts

Project description:The AP-1 transcription factor subunit Junb acts as a context-dependent transcriptional regulator. While positive regulatory functions of Junb are widely studied, the mechanism by which Junb exerts negative regulatory functions remains unclear. miRNAs could translate repressor functions of Junb. Therefore, the aim of this study was to identify Junb-dependent miRNAs in immortalized fibroblasts (MEFs) derived from murine Junb knock-out and wildtype embryos. Cells were published previously in Licht et al. (2010) J Clin Invest. 120(7):2307-18.

2015-10-13 | GSE43380 | GEO

JunB overexpression effect on microvascular endothelial cell culture

Project description:Analysis of gene expression in immortalized human microvascular endothelial cells (TIME cells) following forced expression of the JunB. Results provide insight into a role for the JunB signaling pathway in endothelial cell.

2017-01-31 | GSE93616 | GEO

RNA-Seq JunB WT and KO Tregs Mus musculus

Project description:To understand the mechanisms through which JunB regulates Tregs-mediated immune regulation, we examined the global gene expression profiles in the JunB WT and KO Tregs by performing RNA sequencing (RNA-seq) analysis.

2019-05-07 | GSE129060 | GEO

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