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Expression data from Minoxdil, Keratin and microsphere keratin in vivo

ABSTRACT: Gene expression profiling reveals a potential effect of microsphere keratin in stimulating hair growth in vivo Mice back was depilated and then treated with 1% milliQ, 1% minoxidil, 1% keratin, 1% microsphere keratin for 20 days. Then the skin was collected and RNA was extracted from thetreatd skin as explained in the following section. The microarray was conducted for two biological replicates

ORGANISM(S): Mus musculus Mus

PROVIDER: GSE217935 | GEO | 2022/11/15

REPOSITORIES: GEO

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Keratins control Nrf2 by regulating mitochondrial activity and barrier composition / Keratin-dependent TSLP expression suggests a link between skin blistering and atopic disease

Project description:The epidermal barrier protects the body against mechanical injury, infection and dehydration. The respective contribution of type I and type II keratins which form the major cytoskeleton in epidermal keratinocytes in barrier formation and stress protection is incompletely understood. Here, we reveal a novel mechanism by which keratins control anti-oxidant responses through barrier-dependent and cell-autonomous mechanisms. Mice lacking the entire type I (KtyI) or type II (KtyII) keratin gene clusters suffer from distinct prenatal barrier defects. Comparative transcriptome profiling identifies essential cornified envelope components and reveals strong upregulation of the bZIP transcription factor Nrf2 in situ. Isolated keratinocytes from both strains of mice show elevated mitochondrial oxygen consumption and Nrf2 activity, decreased upon keratin re-expression. We propose a model in which keratins control mitochondria-derived oxidative stress via Nrf2 activation. Our findings reveal major contributions of keratins to chronic inflammation and autoimmune disorders. Total RNA obtained from E18.5 embryo back skin from typeI and II keratin knockout compared with respective wild type.

2016-03-26 | E-GEOD-79590 | biostudies-arrayexpress

Folding Keratin Gene Clusters During Skin Specification

Project description:Folding Keratin Gene Clusters During Skin Specification

| PRJNA561632 | ENA

Folding Keratin Gene Clusters During Skin Specification

Project description:Regional specification is critical for skin development, regeneration and evolution. The contribution of epigenetics in this process remains unknown. Here using avian epidermis we find two major strategies regulate β-keratin gene clusters. 1) Over the body, macro-regional specificities (scales, feathers, claws, etc) established by typical enhancers control five sub-clusters located within the epidermal differentiation complex on chromosome 25; 2) Within a feather, micro-regional specificities are orchestrated by temporo-spatial chromatin looping of the feather β-keratin gene cluster on chromosome 27. Analyses suggest a 3-factor model for regional specification: competence factors (e.g., AP1) make chromatin accessible, regional specifiers (e.g., Zic1) target specific genome regions, and chromatin organizers (e.g., CTCF, SATB2) establish looping configurations. Gene perturbations disrupt morphogenesis and histo-differentiation. This chicken skin paradigm advances our understanding of how regulation of big gene clusters can set up a two-dimensional body surface map.

2020-06-08 | GSE136224 | GEO

Induction of inflammatory cytokines by a keratin mutation in a mouse model for EBS

Project description:Epidermolysis bullosa simplex (EBS) is a skin disorder caused by mutations in keratin (K) 5 or K14 genes. It is widely regarded as a mechanobullous disease, resulting from a weakened cytoskeleton, causing extensive cytolysis. It was postulated by others that certain K14 mutations induce TNF-alfa and increase apoptosis. Here, we report that in K5-/- mice , the mRNA and protein levels of TNF-alfa remain unaltered. Transcriptome analysis of K5-/- mice revealed however, that the pro-inflammatory cytokines interleukin-6 and interleukin-1beta were significantly upregulated at the mRNA level in K5-/- mouse skin. These results were confirmed by TaqMan real-time PCR and ELISA assays. We hypothesize that keratin mutations contribute to EBS in a mouse model by inducing local inflammation that mediates a stress response. Keywords: comparative gene expression profile

2007-05-01 | GSE7663 | GEO

Quantitative phosphoproteomic analysis reveals system-wide signaling pathways regulated by site-specific phosphorylation on Keratin-8 in skin squamous cell carcinoma derived cell-line

Project description:The epithelial specific keratin pair, Keratin 8/18 (K8/18), has been reported to be aberrantly expressed in squamous cell carcinoma (SCC) which is also correlated with increased invasiveness and poor prognosis. A Majority of Keratin 8 (K8) functions are governed by its phosphorylation at Serine73 (head domain) and Serine431 (tail domain) residues. Although deregulation of K8 phosphorylation has been associated with progression of different carcinomas, its role in skin SCC and the underlying mechanism is obscured. To understand the molecular basis of K8 phosphorylation mediated regulation of skin SCC progression, we performed TMT-based quantitative phosphoproteomics by expressing K8 wild type, phosphodead and phosphomimetic mutants in K8 deficient A431 cells. Bioinformatic analysis of our phosphoproteomic data showed differential regulation of phosphoproteins associated with migratory, proliferative and invasive potential in these cells. Further validation of protein phosphorylation levels and phenotypic validation of our phosphoproteomic data suggested potential role of K8 site specific phosphorylation/dephosphorylation in neoplastic progression of A431 cells.

2018-07-05 | PXD005301 | Pride

Transcription profiling of mouse model of Epidermolysis bullosa simplex (EBS) K5-/- skin reveals induction of inflammatory cytokines by a keratin mutation

2008-06-15 | E-GEOD-7663 | biostudies-arrayexpress

Dkk4 and Eda regulate distinctive developmental mechanisms for subtypes of mouse hair-1

Project description:Dkk4 transgenic mice in wild-type background showed abnormal hair subtype formation. Gene expression profiling showed significant down regulation of hair follicle-related keratin genes and hair keratin-associated protein genes at E18.5 and P1. Keywords: development or differentiation design,genetic modification design To define target genes of Dkk4 during hair follicle development, we carried out microarray experiments with mouse back skin samples that from 4 developmental time points including E14.5, E16.5, E18.5 and P1 of wild-type and wild-type background Dkk4 transgenic mice.

2010-09-03 | E-GEOD-19309 | biostudies-arrayexpress

Genome-wide analysis of gene expression in Krt1+/+ versus Krt1-/- epidermis and full-thickness skin.

Project description:Keratin 1 (KRT1) and its heterodimer partner keratin 10 (KRT10) constitute the intermediate filament cytoskeleton of suprabasal skin keratinocytes. They participate in formation of the epidermal barrier, which protects against dehydration and inflammation. Mutations in KRT1 cause keratinopathic ichthyosis with erythema, recurrent inflammation, and barrier defects. Here, we show that genetic deletion of Krt1 in mice causes a defective inside-out epidermal barrier, pre- and postnatal increases in Mrp8/Mrp14, interleukin (IL) 18, IL-33, and thymic stromal lymphopoietin (TSLP) in skin extracts, and systemic release of IL-18 into newborn serum. Perinatal lethality was partially rescued by treatment with glucocorticoids to promote barrier repair or with IL- 18-blocking antibodies in utero. In human keratinocytes, IL-18 release was cellautonomous and caspase-1-dependent, indicating KRT1-dependent inflammasome activation. Our data reveal a novl function of KRT1 in controlling inflammasome activity and stimulating barrier formation, thereby integrating the keratin cytoskeleton into the epidermal immune response. In view of their widespread expression, keratins merit investigation of their functions in inflammatory conditions, including asthma and inflammatory bowel disorders. Total RNA was obtained from epidermis or full-thickness skin of Krt1+/+ and Krt1-/- mice (C57BL/6 background) at P0 (newborn).

2012-12-01 | E-GEOD-32951 | biostudies-arrayexpress

Community-intrinsic properties enhance keratin degradation from bacterial consortia

Project description:We studied the microbial community-based degradation of keratin, a recalcitrant biological material, by four well-characterized synergistic soil isolates, which have previously been shown to display synergistic interactions during biofilm formation; Stenotrophomonas rhizophila, Xanthomonas retroflexus, Microbacterium oxydans and Paenibacillus amylolyticus. We observed enhanced keratin weight loss in cultures with X. retroflexus, both in dual and four-species co-cultures, as compared to expected keratin degradation by X. retroflexus alone. To unravel the degradation shotgun-proteomics was performed on the secretome of all culture types including X. retroflexus.

2020-02-18 | PXD016745 | Pride

Regional specific differentiation of integumentary organs: SATB2 is involved in α- and β-keratin gene cluster switching in the chicken

Project description:Animals develop skin regional specificities to best adapt to their environments. Birds are excellent models in which to study the epigenetic mechanisms that facilitate these adaptions. Patients suffering from SATB2 mutations exhibit multiple defects including ectodermal dysplasia-like changes. The preferential expression of SATB2, a chromatin regulator, in feather-forming compared to scale-forming regions, suggests it functions in regional specification of chicken skin appendages by acting on either differentiation or morphogenesis. Retrovirus mediated SATB2 misexpression in developing feathers, beaks, and claws causes epidermal differentiation abnormalities (e.g. knobs, plaques) with few organ morphology alterations. Chicken β-keratins are encoded in 5 sub-clusters (Claw, Feather, Feather-like, Scale, and Keratinocyte) on Chromosome 25 and a large Feather keratin cluster on Chromosome 27. Type I and II α-keratin clusters are located on Chromosomes 27 and 33, respectively. Transcriptome analyses showed these keratins 1) are often tuned up or down collectively as a sub-cluster, and 2) these changes occur in a temporo-spatial specific manner. This cluster-level suppression is also seen in MMPs on Chromosome 1. SATB2 alters gene expression changes of most other transcripts without this cluster-level switching. These results suggest an organizing role of SATB2 in cluster-level gene co-regulation during skin regional specification.

2021-08-14 | GSE178651 | GEO

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