Ontology highlight
ABSTRACT:
PROVIDER: PRJNA453372 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7059800_1.fastq.gz | Fastqsanger.gz | |||
| SRR7059800_2.fastq.gz | Fastqsanger.gz | |||
| SRR7059801_1.fastq.gz | Fastqsanger.gz | |||
| SRR7059801_2.fastq.gz | Fastqsanger.gz |
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Project description:JunB defines functional and structural integrity of the epidermo-pilosebaceous unit in the skin
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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.
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Project description:Salamanders, such as the Mexican axolotl, are some of the few vertebrates fortunate in their ability to regenerate diverse structures after injury. Unlike mammals they are able to regenerate a fully functional spinal cord after injury. Throughout human life, many cells and certain tissues, such as hair follicle stem cells and liver, can be continuously replaced to maintain functional integrity in response to normal daily wear and tear. However, the human response to more serious tissue damage is limited to relatively primitive wound healing, whereby collagenous scar tissue fills the injury site, assuring the tissue’s structural integrity but often resulting in a debilitating loss of functionality. In contrast many vertebrates, including axolotls, have remarkable regenerative capacity including the functional regeneration of full thickness wounds. Here, we have identified a novel role for SALL4 in regulating collagen transcriptional after injury that is essential to ensure perfect skin regeneration in axolotl.
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Project description:T cells coordinate with structural cells in the skin to promote appropriate inflammatory responses and subsequent restoration of barrier integrity following insult. Single cell studies of human skin have defined an assortment of transcriptionally distinct structural cell populations in healthy tissue and identified inflammatory disease-associated changes in epithelial keratinocytes and dermal fibroblasts. Cutaneous T lymphocyte activity is implicated in the development of inflammatory skin disease, but the mechanisms by which T cells promote disease-associated changes in the skin remain unclear. We show that distinct subsets of circulating and resident CD4+ cutaneous T cells promote a diverse array of transcriptional outcomes in human keratinocytes and fibroblasts. Using these in vitro generated transcriptional signatures, we identify T cell-dependent gene modules associated with inflammatory skin diseases in vivo, such as a set of Thelper17 cell-induced genes in keratinocytes that are enriched in the skin of patients with psoriasis and normalized in response to anti-IL-17 therapy. Thus, we present an approach to define the immune-dependent gene networks of skin structural cells, which we use to study the T cell contribution to inflammatory skin disease and response to anti-cytokine therapy.
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Project description:The ErbB famliy of erceptor tyrosine kinases and their ligands, neuregulins(NRGs), are crtical involved not only in cardiac development but also in the maintenace of structural and functional integrity of the adult heart. rhNRG-1(recombinant human NRG-1) Improves cardiac function and sruvival in models of ischemic, dilated, and viral cardiomyopathy with the ErbB-activation. But the mechanism is still unknown Keywords: Genechips
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Project description:Barrier integrity is central to the maintenance of a healthy immunological homeostasis. Impaired skin barrier function is linked with enhanced allergen sensitization and the development of diseases such as atopic dermatitis (AD), which can precede the development of other allergic diseases such as food allergies and asthma. Epidemiological evidence indicates that children suffering from allergies have lower levels of dietary fibre-derived short-chain fatty acids (SCFA). Using an experimental model of AD, we report that a fermentable fibre-rich diet alleviates AD severity and systemic allergen sensitization. The gut-skin axis underpins this phenomenon through SCFA, which strengthen skin barrier integrity by altering mitochondrial metabolism of epidermal keratinocytes. SCFA promote keratinocyte differentiation and the production of key structural lipids, resulting in enhanced barrier function. Our results demonstrate that dietary fibre and SCFA mitigate AD by improving barrier integrity, ultimately limiting early systemic allergen sensitization and development of disease.
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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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