E-MTAB-3836
Ontology highlight
ABSTRACT:
PROVIDER: E-MTAB-3836 | ExpressionAtlas | 2015-08-25
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-MTAB-3836-analysis-methods.tsv | Tabular | |||
| E-MTAB-3836-atlasExperimentSummary.Rdata | Rdata | |||
| E-MTAB-3836-configuration.xml | Xml | |||
| E-MTAB-3836-percentile-ranks.tsv | Tabular | |||
| E-MTAB-3836.condensed-sdrf.tsv | Tabular |
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Project description:Analysis of ex vivo isolated lymphatic endothelial cells from the dermis of patients to define type 2 diabetes-induced changes. Results preveal aberrant dermal lymphangiogenesis and provide insight into its role in the pathogenesis of persistent skin inflammation in type 2 diabetes. The ex vivo dLEC transcriptome reveals a dramatic influence of the T2D environment on multiple molecular and cellular processes, mirroring the phenotypic changes seen in T2D affected skin. The positively and negatively correlated dLEC transcripts directly cohere to prolonged inflammatory periods and reduced infectious resistance of patients´ skin. Further, lymphatic vessels might be involved in tissue remodeling processes during T2D induced skin alterations associated with impaired wound healing and altered dermal architecture. Hence, dermal lymphatic vessels might be directly associated with T2D disease promotion. Global gene expression profile of normal dermal lymphatic endothelial cells (ndLECs) compared to dermal lymphatic endothelial cells derived from type 2 diabetic patients (dLECs).Quadruplicate biological samples were analyzed from human lymphatic endothelial cells (4 x diabetic; 4 x non-diabetic). subsets: 1 disease state set (dLECs), 1 control set (ndLECs)
2012-06-01 | E-GEOD-38396 | biostudies-arrayexpress
Project description:Analysis of ex vivo isolated lymphatic endothelial cells from the dermis of patients to define type 2 diabetes-induced changes. Results preveal aberrant dermal lymphangiogenesis and provide insight into its role in the pathogenesis of persistent skin inflammation in type 2 diabetes. The ex vivo dLEC transcriptome reveals a dramatic influence of the T2D environment on multiple molecular and cellular processes, mirroring the phenotypic changes seen in T2D affected skin. The positively and negatively correlated dLEC transcripts directly cohere to prolonged inflammatory periods and reduced infectious resistance of patients´ skin. Further, lymphatic vessels might be involved in tissue remodeling processes during T2D induced skin alterations associated with impaired wound healing and altered dermal architecture. Hence, dermal lymphatic vessels might be directly associated with T2D disease promotion.
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Project description:Skin undergoes changes in structure and function with age, including a shift in metabolic programs. This is particularly evident relative to mitochondrial function in skin cells. Dermal fibroblasts have been known to accumulate damage caused by both external and internal stressors, leading to altered bioenergetics that limits efficient synthesis of ATP and NAD+. To better understand the changes in mitochondrial function with age, metabolic profiles and transcriptomic profiles of primary dermal fibroblasts from varying aged donors were analysed.
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Project description:we report that regional expression of the Hoxc genes is regulated by antagonistic switch between repression and activation epigenetic modification. In freshly isolated dermal cells from P50 telogen Wt/Wt ear skin, no enrichment of H3K27ac was detected at Hoxc cluster, consistent with their lack of expression; in contrast, robust peaks of this marker are observed in 3’ region of the Hoxc cluster in dorsal skin dermal cells. Secondly we looked at H3K27 trimethylation (H3K27me3), a marker for polycomb-dependent gene repression, which antagonizes H3K27ac. Concomitantly, we found that H3K27me3 spread across the entire Hoxc cluster in adult ear skin dermal cells but was restricted to the 5’ region of the Hoxc cluster in adult dorsal skin dermal cells . In adult dorsal skin dermal cells, we found three occupied CTCF binding sites inside Hoxc cluster. The rostral CTCF binding site marks the discontinuity point of H3K27me3 modification at the intergenic region between Hoxc11 and Hoxc10 in dorsal skin dermal cells. This indicates the CTCF binding event within Hoxc cluster might forge a topological barrier that can insulate activation region from repression region and therefore lead to the region specific expression of the Hoxc cluster genes.To directly test whether there is ectopic interaction between Hoxc cluster and the active domain in proximal-TAD, we used circularized chromosome conformation capture (4C) with Hoxc4 as bait. In Wt/Koa ear skin dermal cells, there are clear ectopic interactions of Hoxc4 with the remaining active regulatory landscape in proximal-TAD; on the other hand, all of the interactions of Hoxc4 remained inside the distal-TAD with repressive domain in Wt/Wt ear skin.
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Project description:Global expression analysis of neural crest-like skin-derived precursors (SKPs) and Sox2-positive follicle dermal cells that SKPs originate from. In spite of the remarkable regenerative capacity of mammalian skin, an adult dermal stem cell has not yet been identified. Here, we provide evidence that SKPs, multipotent neural crest-like skin-derived precursors, represent an adult dermal stem cell. When transplanted into adult skin, SKPs can reconstitute the adult dermis, contribute to dermal wound-healing, home to a hair follicle niche, and instruct epidermal cells to make hair follicles. Hair follicle-derived SKPs self-renew, maintain their multipotency, and serially reconstitute hair follicles. The endogenous origin of SKPs are Sox2-positive follicle dermal cells that share a similar global gene expression profile with SKPs. These endogenous cells home back to their follicle niche, induce hair follicle morphogenesis, and differentiate into neural and dermal progeny. Hair follicle-associated dermal cells will move out of their niche to contribute to dermal maintenance and wound-healing. These studies therefore identify a dermal stem cell, and provide a biological rationale for the presence of a multipotent precursor within adult dermis, findings with important therapeutic implications.
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Project description:Primary outcome(s): <Assessment by devices> 1) Optical properties (absorption and scattering coefficients) 2) Spectral reflectivity 3) Visia (Facial skin condition) 4) Epidermal and dermal water content <Self-completed questionnaires> Appearance-related distress
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Project description:Objectives: Eph/Ephrin cell-cell signaling is emerging as a key player in tissue fibrogenesis. The aim of this study was to test the hypothesis that the receptor tyrosine kinase EphB2 mediates dermal fibrosis in systemic sclerosis (SSc). Methods: We assessed normal and SSc human skin biopsies for EphB2 expression. The in vivo role of EphB2 in skin fibrosis was investigated by subjecting EphB2-knockout mice to both bleomycin-induced and tight skin (Tsk1/+) genetic mouse models. EphB2 kinase-dead and overactive point mutant mice were used to evaluate the role of EphB2 forward signaling in bleomycin-induced dermal fibrosis. In vitro studies were performed on dermal fibroblasts from SSc patients and healthy controls, which was followed by in vivo analysis of fibroblast-specific EphB2 deficient mice. Results: Expression of EphB2 is upregulated in SSc skin tissue and explanted SSc dermal fibroblasts compared to healthy controls. EphB2 expression is elevated in two animal models of dermal fibrosis. In mice, EphB2 drives dermal fibrosis in both the bleomycin and the Tsk1/+ models of skin fibrosis. EphB2 forward signaling is a critical mediator of dermal fibrosis. Transforming growth factor-β (TGFβ) cytokines upregulate EphB2 in dermal fibroblasts via non-canonical TGFβ/SMAD signaling and silencing EphB2 in dermal fibroblasts is sufficient to dampen TGFβ-induced fibroblast-to-myofibroblast differentiation. Moreover, mice with fibroblast-specific deletion of EphB2 showed impaired fibroblast-to-myofibroblast differentiation and reduced skin fibrosis upon bleomycin challenge. Conclusion: Our data implicate EphB2 overexpression and kinase-mediated forward signaling in the development of dermal fibrosis in SSc. EphB2 thus represents a potential new therapeutic target for SSc.
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Project description:Different types of hair follicles can be found in the skin of mice. It is believed that the signals that control hair follicle differentiation arise from cells in a structure called the dermal papilla. Understanding the nature of those signals is of interest for the biology of the normal tissue. We have developed a technique for isolation of dermal cells by enzymatic digestion of intact skin. We have identified two subpopulations of cells that can be separated by FACS. The Sox2-positive CD133-positive cells are found exclusively in the dermal papillae of guard/awl/auchene hairs, while Sox2-negative, CD133-positive cells are found in the other hair follicle types. We compared these populations with unfractionated dermal cells. We isolated the following 3 populations of cells from the back skin of neonatal mice (P2) by Flow Cytometry: 1) GFP-CD133- Total dermal cells 2) GFP-CD133+ Dermal Papilla cells 3) GFP+CD133+ Dermal Papilla cells The yield is approximately 50,000 cells of each population.
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