Stump project-- mRNA basal layer keratinocytes; Volar versus non-volar acral skin gene expression
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Luis Garza
PROVIDER: E-GEOD-39500 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:We were interested in defining the gene signature of volar skin. Punch biopsies of skin were split into epidermis and dermis after dispase treatment. We collected RNA from epidermis of palms, backs of hand, soles and backs of feet and submitted for Affymetrix Exon arrays. 3 replicates of each site from distinct human donors were included; total of 12 samples analyzed
2013-07-03 | E-GEOD-39267 | biostudies-arrayexpress
Project description:We were interested in defining the gene signature of volar skin. Punch biopsies of skin were split into epidermis and dermis after dispase treatment. We collected RNA from dermis of palms, backs of hand, soles and backs of feet and submitted for Affymetrix Exon arrays. 3 replicates of each site from distinct human donors were included; total of 12 samples analyzed
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Project description:We were interested in defining the gene signature of volar skin. Dermal fibroblasts were expanded from punch biopsies of skin. We collected RNA from fibroblasts of palms, backs of hand, soles and backs of feet and submitted for Affymetrix Exon arrays. 3 replicates of each site from distinct human donors were included; because of 1 failed sample(Palm_rep2), total of 11 samples analyzed
2013-07-03 | E-GEOD-39266 | biostudies-arrayexpress
Project description:We were interesed in defining the gene signautre of volar skin. Whole skin punch biopsies of palms, backs of hand, soles and backs of feet were submitted for Affymetrix Exon arrays. 4 replicates of each site from distinct human donors were included; total of 16 samples analyzed.
2013-07-01 | E-GEOD-34756 | biostudies-arrayexpress
Project description:Analysis of microRNA expression in keratinocytes by relative quantification (RQ) using the comparative Ct method. Real-time quantitative PCR analysis of microRNA in keratinocytes or reconstituted epidermis exposed to IL-22, LPS or UV radiation or a small molecule drug. Keratinocytes or reconstituted human epidermis were exposed to indicated treatments. A qPCR analysis of 365 microRNAs in keratinocytes. RNA (20 ng per reaction) reverse transcribed using 8 x Multiplex RT pools. Each resulting cDNA pool was mixed with TaqMan Universal PCR Master Mix and loaded in corresponding port on the TaqMan Array.
2013-05-23 | E-GEOD-41838 | biostudies-arrayexpress
Project description:Transcriptional coactivator Mediator complex facilitates transcription of various transcription factors. Previously, we have generated Med1 conditional null mice, where a critical subunit of Mediator, Med1, is removed from keratinocytes. Here we present evidence that ablation of Med1 accelerated epidermal regeneration after injury. As bulge keratinocyte stem cells are important contributors to regenerate epidermis, we first analyzed properties of stem cells in Med1 null mice. BrdU long retaining analysis revealed that deletion of Med1 still maintained quiescence of bulge keratinocyte stem cells, despite of general hyperplasia observed in Med1 deficient keratinocytes. Gene expression analysis demonstrated that a series of niche matrix proteins decreased in Med1 deficient keratinocytes. In contrast, the expression of stem cell marker Sox9 was not altered, suggesting stem cells are present but activated because of abnormal niche surrounding stem cells. In addition, Med1 deletion suppressed injury induced inflammatory reaction, which indirectly regulates epidermal regeneration. We also indicated that TGFβ1 significantly decreased in both bulge and epidermal keratinocytes upon Med1 deletion. Our study demonstrates that coactivator Med1 has a critical role to maintain bulge stem cells and epidermal regeneration presumably through regulation in TGFβ signaling. n=3 WT and KO (each group contains keratinocytes isolated from adult skins excised from 2 mice)
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Project description:The aim of this study was to analyze the in vitro biological epidermal processes occurring in reconstructed skins using cells from breast skin of African and Caucasian skin type color. A exploration of mRNA expression levels in the epidermis of reconstructed skin was undertaken to elucidate the differential in vitro functions of keratinocytes. The reconstruction of skin models was made with keratinocytes and fibroblasts from four different donors per skin type and experiments were conducted in triplicate for each donor. At the end of culture, the epidermis from reconstructed skin was manually separated from the dermal equivalent part in order to analyse gene expression in keratinocytes only. RNA samples were labelled with biotin and hybridation was performed on Affymetrix Human Genome U133 + PM Array Plates.
2020-08-10 | E-MTAB-9433 | biostudies-arrayexpress
Project description:Expression of enzymatically inactive caspase-8, or deletion of caspase-8 from basal epidermal keratinocytes, triggers chronic skin inflammation in mice. Unlike similar inflammation resulting from arrest of NF-kB activation in the epidermal cells, the effect induced by caspase-8 deficiency did not depend on TNF, IL1, dermal macrophage function, or expression of the Toll-like receptor adapter proteins MyD88 or TRIF. Both interferon regulatory factor (IRF)3 and TANK-binding kinase were constitutively phosphorylated in the caspase-8-deficient epidermis, and knockdown of IRF3 in the epidermis-derived cells from these mice abolished the expression of upregulated genes. Temporal and spatial analyses of the alterations in gene expression that result from caspase-8 deficiency reveal that the changes are initiated before birth, around the time that cornification develops, and occur mainly in the suprabasal layer. Finally, we found that caspase-8-deficient keratinocytes display an enhanced response to gene activation by transfected DNA. Our findings suggest that an enhanced response to endogenous activators of IRF3 in the epidermis, presumably generated in association with keratinocyte differentiation, contributes to the skin inflammatory process triggered by caspase-8 deficiency. Epidermal keratinocytes were isolated from the skin of Casp-8F/M-bM-^@M-^SK5-Cre or Casp-8F/+K5-Cre mice. Keratinocyte samples from two mice of each genotype were isolated and subsequently cultured. Total RNA was extracted at the first and the third passage of cultivation (8 RNA samples originated in total). The appropriate pairs of RNA samples suited for a direct comparison of the two different genotypes under examination were differently labeled and subsequently co-hybridized onto one microarray (dual color design).
2009-07-29 | E-GEOD-17345 | biostudies-arrayexpress
Project description:The vitamin D receptor (VDR) regulates cell proliferation and differentiation including epidermal keratinocytes by modulating transcription of its target genes. We are investigating the role of VDR in epidermal stem cells and their progenies in the regeneration process of epidermis and hair in the skin. VDR null mice are utilized in which VDR is specifically deleted in keratin 14 (K14) expressing keratinocytes by Cre-lox strategy. The impact of VDR deletion was evaluated by comparison of VDR null mice with no cre littermate control mice. The VDR was abundantly expressed in potential epidermal stem cells including basal cells in interfollicular epidermis (IFE), and in CD34 expressing bulge keratinocytes in hair follicles. Gene expression profiles and subsequent pathway analysis of stem cell enriched keratinocyte populations revealed that the VDR deletion significantly suppressed β-catenin signaling as well as VDR signaling. The role of VDR in epidermal stem cells was studied during hair follicle cycling and wound healing processes. The epidermal stem cells were not appropriately stimulated by hair depilation, and did not reinitiate anagen in the hair follicles resulting in a failure of hair regrowth. In addition, the stem cells were not fully activated after full thickness wounds were generated in VDR null skin under a low calcium diet to suppress compensation pathways. Cell proliferation was not fully induced in potential stem cells located in both IFE and hair follicles near the wounding edges, and re-epithelialization rate was delayed in VDR null skin. Gene expression profiling of the wounded skin (3 days after injury) indicated that β-catenin signaling was not fully induced in VDR null skin comparable to that observed in β-catenin null mice. The β-catenin target genes including Axin2 and cell cycle regulators involved in epidermal stem cell function were not induced in the edges of the wound of VDR null skin. These results demonstrated that VDR plays an essential role in hair cycling and wound healing processes through regulation of β-catenin signaling in epidermal stem cells and their progenies. n=3 CON and KO (each sample contain RNA extracted from keratinocytes, which is isolated from VDR KO and littermate control skins excised from 3 mice)
2015-07-31 | E-GEOD-68729 | biostudies-arrayexpress
Project description:Calcium and 1,25-dihydroxyvitamin D3 (1,25D3), through the actions of their respective receptors, the Ca2+-sensing receptor (CaSR) and the vitamin D receptor (VDR), potentiate keratinocyte differentiation. VDR regulates epidermal keratinocyte proliferation and differentiation by modulating gene transcription, whereas the CaSR, a member of the family C G-protein coupled receptor, calcium mobilizes intracellular calcium and induces the formation of cell-cell junctions. 1,25D3 augments the sensitivity of the prodifferentiating actions of calcium by increasing the expression of CaSR. CaSR- and VDR-deficient keratinocytes share common characteristics such as abnormal intercellular adhesion and sphigolipid metabolism. Both CaSR and VDR are abundantly expressed in epidermal stem cell populations including CD34 expressing bulge keratinocytes in hair follicles and basal cells in interfollicular epidermis. To delineate the role of CaSR- and VDR-dependent pathways in regulating epidermal development and functions in physiological state, we generated conditional CaSR-null and VDR-null mice, where Casr and VDR gene was removed from keratinocytes. Keratinocyte-specific CaSR-null and VDR-null mice manifest distinct phenotypes. CaSR-null mice display defective epidermal permeability barrier function due to aberrant keratinocyte differentiation. VDR-null mice develop alopecia after completing the first hair follicle cycling. Concurrent ablation of CaSR and VDR genes in keratinocytes delays rate of wound repair and increases incidence of skin tumor formation to a greater extent than deletion of the CaSR or VDR alone, indicative of synergistic effects of calcium and 1,25D3 signaling. Gene expression profiles and subsequent pathway analysis on the epidermis derived from 5-day-old neonates revealed that ablation of CaSR or VDR increased expression of genes associated with cancer progression and metastasis. Deletion of VDR markedly inhibited signaling pathways that regulate hair development. Furthermore, concurrent ablation of CaSR and VDR significantly suppressed calcium, VDR, Wnt/b-catenin signaling, as well as epithelial adherence junction signaling to maintain appropriate keratinocyte adhesion. These results indicated the interplay of calcium/CaSR and 1,25D3/VDR signaling in keratinocyte proliferation and differentiation, and their importance in maintaining normal epidermal adhesion and functions. n=3 CON and KO (each sample contain RNA isolated from neonatal epidermis separated from 3 mice)
2015-07-31 | E-GEOD-68723 | biostudies-arrayexpress