MicroRNA expression in skin and wound edge tissue at different time points
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Chandan Sen
PROVIDER: E-GEOD-55661 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:We uncover a novel mechanism whereby developmental pathways are reactivated in adults to promote regeneration.
2019-05-23 | PXD013854 | Pride
Project description:The expression profile during wound repair of cutaneous excisional wound (2x2 cm) was studied. The tissue was sampled from the centre of the open wound (day 3/7/14) or centre of the wound scar (day 21/35/70). The microarray slide were scanned in low intensity scan and high intensity scan mode. Wound tissue (day 3, day 7, day 14, day 21, day 35, day 70, n = 4 per interval) vs. control - uninjured skin (day 0, n=4 ). In each interval two biological replicates of four were labeled with flip dyes.
2012-07-29 | E-GEOD-37947 | biostudies-arrayexpress
Project description:To study early-onset gene expression changes in cutaneous wound healing, 3 mm wounds were induced into the back skin of female wildtype C57BL/6 mice using a biopsy punch. Mice were sacrificed 2h, 6h or 24h post wound induction (PWI) and 1 - 1.5 mm of skin lining the wound edge was isolated and sequenced. The skin from the initial punch biopsy (0h PWI) was preserved and taken as a control sample to identify differentially expressed genes.
2018-07-31 | E-MTAB-6686 | biostudies-arrayexpress
Project description:The full complement of hair follicles is generated during embryogenesis. Normally, no new hair is created after this time. Large full thickness skin excision wounding can result in the generation of new hair in the adult. Placodes can be observed following complete reepithelialization at wound day 14. The events leading to hair neogenesis following wounding remain poorly understood. Late healing events (from wound day 10 to wound day 14) provide a possible window of induction for hair regeneration. We used microarrays to analyse changes in gene expression during late skin healing to provide candidates for factors involved in hair neogenesis following wounding. 6 week old C57Bl/6 mice received large full thickness skin excisions. Healing wound tissue was excised at wound day 10, 12 or 14 and analyzed for gene expression.
2013-09-01 | E-GEOD-46244 | biostudies-arrayexpress
Project description:Studying the transcriptomic response of different epidermal stem cell populations to wounding has been difficult due to intermixing of wound healing and homeostastic cells from different stem cell pools in bulk-cell sequencing setups. Here, we circumvent those problems by using a single-cell sequencing approach. We randomly sequenced the traced progeny of either Lgr5 or Lgr6 stem cells isolated from wounded or unwounded skin 0 day (control), 1 d, 4 d, 7 d, 10 d or more than 1 month after wounding. We then identified Lgr5 or Lgr6 wound cells using a computational approach. Wound cells were defined by using a negative binominal Naïve Bayes classifier with 0-day control cells (unwounded mice) as reference. Wound cell populations were defined by clustering wound cells in t-SNE space using k-means clustering.
2018-04-01 | E-MTAB-6583 | biostudies-arrayexpress
Project description:Nonsyndromic cleft palate is a common birth defect (1:700) with a complex etiology involving both genetic and environmental risk factors. Nicotine, a major teratogen present in tobacco products, was shown to cause alterations and delays in the developing fetus. To demonstrate the effect of nicotine on craniofacial development, particularly palatogenesis, we delivered three different doses of nicotine (1.5, 3.0 and 4.5 mg/kg/day) into pregnant BALB/c mice throughout their entire pregnancy using subcutaneous osmotic mini-pump. We assessed the pups for morphological anomalies, as well as genome-wide mRNA (transcriptome) microarray analysis. Consistent administration of nicotine caused developmental retardation, still birth, low birth weight, and significant palatal size and shape abnormality in the pups. However, it did not cause obvious cleft palate. The microarray data analysis using IPA identified differential expression of genes involved in various biological pathways, particularly cancer, genetic diseases, and tissue development in response to consistent nicotine exposure. 6232 up-regulated and 6310 down-regulated genes were detected in nicotine-treated groups compared to the control. Moreover, 45% of the genes associated with cleft palate were found to be affected by nicotine. Alterations of a subset of differentially expressed genes were illustrated with hierarchal clustering and RT-PCR. We concluded that consistent nicotine exposure during pregnancy interferes with normal growth and development of the fetus including palatogenesis; however, this interference does not result in cleft palate, rather smaller palate size with persistent MES. To our knowledge, this is the first experiment revealing the impact of nicotine on the fetal palate transcriptome in mice. Total 8 samples were analyzed. Using an osmotic minipump, duplicate samples from palates of either sterile physiological saline or nicotine (1.5 mg/kg/day, 3.0 mg/kg/day, or 4.5 mg/kg/day)-treated newborn pups.
2011-12-15 | E-GEOD-31004 | biostudies-arrayexpress
Project description:Diet High in salt content have been associated with cardiovascular disease and chronic inflammation. We recently demonstrated that transient receptor potential canonical 3 (TRPC3) channels regulate myofibroblast transdifferentiation in hypertrophic scars. Here, we examined how high salt activation of TRPC3 participates in hypertrophic scarring during wound healing. In vitro, we confirmed that high salt increased the TRPC3 protein expression and the marker of myofibroblast alpha smooth muscle actin (α-SMA) in wild-type mice (WT) primary cultured dermal fibroblasts but not Trpc3-/- mice. Activation of TRPC3 by high salt elevated cytosolic Ca2+ influx and mitochondrial Ca2+ uptake in dermal fibroblasts in a TRPC3-dependent manner. High salt activation of TRPC3 enhanced mitochondrial respiratory dysfunction and excessive reactive oxygen species (ROS) production by inhibiting pyruvate dehydrogenase action, that activated ROS-triggered Ca2+ influx and the Rho kinase/MLC pathway in WT mice but not Trpc3-/- mice. In vivo, a persistent high-salt diet promoted myofibroblast transdifferentiation and collagen deposition in a TRPC3-dependent manner. Therefore, this study demonstrates that high salt enhances myofibroblast transdifferentiation and promotes hypertrophic scar formation through enhanced mitochondrial Ca2+ homeostasis, which activates the ROS-mediated pMLC/pMYPT1 pathway. TRPC3 deficiency antagonizes high salt diet-induced hypertrophic scarring. TRPC3 may be a novel target for hypertrophic scarring during wound healing.
2023-10-24 | PXD042087 | Pride
Project description:MicroRNAs are small, non-coding RNAs that regulate gene expression post-transcriptionally. Here, we show that miR-210 is induced by Oct-2, a key transcriptional mediator of B-cell activation. Germline deletion of miR-210 results in the development of autoantibodies from 5 months of age. Overexpression of miR-210 in vivo resulted in cell autonomous expansion of the B1 lineage and impaired fitness of B2 cells. Mice over-expressing miR-210 exhibited impaired class-switched antibody responses, a finding confirmed in wild-type B-cells transfected with a miR-210 mimic. In vitro studies demonstrated a defect in cellular proliferation and cell-cycle entry, which was consistent with the transcriptomic analysis demonstrating down-regulation of genes involved in cellular proliferation and B cell activation. These findings indicate that Oct-2 induction of miR-210 provides a novel inhibitory mechanism for the control of B cells and autoantibody production. Splenic B-cells from different mouse strains were stimulated with either anti-IgM, CD40L and IL-4 or LPS for 48 hours Treatments: rest (unstimulated), Fab/Fab2 (=anti-IgM + CD40L + IL-4), LPS. There is no difference between Fab and Fab2 stimulation conditions. The goal of this study was to look for activation-induced microRNA changes upon B-cell activation, of which miR-210 was one of them.
2013-06-21 | E-GEOD-48186 | biostudies-arrayexpress
Project description:Background: The differential expression pattern of microRNAs (miRNAs) during mammary gland development might provide insights into their role in regulating the homeostasis of the breast epithelium. Our aim was to analyse these regulatory functions by deriving a comprehensive tissue-specific combined miRNA and mRNA expression profile of post-natal mouse mammary gland development. We measured the expression of 318 individual murine miRNAs by bead-based flow-cytometric profiling of whole mouse mammary glands throughout a 16-point developmental time course, including juvenile, puberty, mature virgin, gestation, lactation, and involution stages. In parallel whole-genome mRNA expression data were obtained. Results: One third (n = 102) of all murine miRNAs analysed were present during mammary gland development. MicroRNAs were represented in seven temporally co-expressed clusters, which were enriched for both miRNAs belonging to the same family and breast cancer-associated miRNAs. Global miRNA and mRNA expression was significantly reduced during lactation and the early stages of involution after weaning. For most detected miRNA families we did not observe systematic changes in the expression of predicted targets. For miRNA families whose targets did show significant changes, we observed inverse patterns of miRNA and target expression. The datasets are made publicly available and the combined expression profiles represent an important community resource for mammary gland biology research. Conclusions: MicroRNAs were expressed in co-regulated clusters during mammary gland development. Breast cancer-associated miRNAs were significantly enriched in these clusters. The mechanism and functional consequences of this miRNA co-regulation and its correlation with mRNA expression provide new avenues for research into mammary gland biology and generates candidates for functional validation. Developmental time course over 16 time points with 1-3 independent biological replicates per time point and three pairs of technical replicates, 40 samples in total
2010-06-25 | E-GEOD-15055 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
2015-07-31 | E-GEOD-68730 | biostudies-arrayexpress