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Gene expression in mouse proliferative phase wounds in response to alterations in β-Catenin levels [initiated prior to injury].

ABSTRACT: β-Catenin is a regulator of cutaneous wound repair. The expression of genes that are modulated in response to changes in β-Catenin levels initiated prior to injury was investigated during the proliferative phase of repair. We are particularly interested in genes that are modulated (in opposite directions) in response to both the induction ('stabilization') versus downregulation of β-Catenin. To investigate this, conditional β-Catenin stabilized mice (Harada, N., et al. EMBO J. 1999 Nov 1;18(21):5931-42) were injected with either a Cre-expressing adenovirus, or a GFP-expressing control virus, four days prior to injury, and wounds were harvested eight days following injury. For conditional knockdown of β-Catenin, mice generated from a cross between conditional β-Catenin knockdown mice (Brault, V. et al., Development. 2001 Apr;128(8):1253-64), and mice that express a tamoxifen-inducible form of Cre (Hayashi, S., and McMahon, A.P., Dev Biol. 2002 Apr 15;244(2):305-18), were treated with Tamoxifen for five days prior to injury. Wounds were harvested eight days after wounding. This provides insight into gene expression changes that occur during the proliferative stage of cutaneous wound repair in response to changes in β-Catenin levels initiated before/at the time of injury.

ORGANISM(S): Mus musculus

PROVIDER: GSE50152 | GEO | 2018/12/31

REPOSITORIES: GEO

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Gene expression in mouse whole proliferative phase wounds in response to alterations in β-Catenin levels [induced post-injury].

Project description:β-Catenin is a regulator of cutaneous wound repair. The expression of genes that are modulated in response to changes in β-Catenin levels (stabilization and downregulation) in cutaneous mouse wounds, post injury, during the proliferative phase of repair, was investigated. We are particularly interested in genes that are modulated (in opposite directions) in response to both the induction (stabilization) versus downregulation of β-Catenin. To investigate this, conditional β-Catenin stabilized (Harada, N., et al. EMBO J. 1999 Nov 1;18(21):5931-42) mice were injected with either a Cre-expressing adenovirus, or a GFP-expressing control virus, three days following injury, and wounds were harvested eight days post injury. For conditional knockdown of β-Catenin, mice generated from a cross between conditional β-Catenin knockdown mice (Brault, V. et al., Development. 2001 Apr;128(8):1253-64), and mice that express a tamoxifen-inducible form of Cre (Hayashi, S., and McMahon, A.P., Dev Biol. 2002 Apr 15;244(2):305-18), were treated with Tamoxifen for five days, beginning at the third day after injury. Wounds were harvested eight days after wounding. This provides insight into the identities of genes modulated in response to changes in β-Catenin levels during the proliferative stage of cutaneous wound repair.

2018-12-31 | GSE50153 | GEO

Study the epidermal regulation of mesenchymal tissue behavior using a novel rabbit animal model

Project description:In order to identify tissue specific differences in epithelial behavior following injury, we developed a novel animal model of epithelial-restricted injury in the New Zealand White rabbit. A grid of shallow incisional wounds, which extended through the entire epithelium but did not significantly damage the underlying connective tissue, were created on the skin and vaginal mucosa, and samples were taken at various times post-surgery for histology and molecular analysis. All wounds were completely re-epithelialized between 1 and 2 days post-surgery. A microarray analysis was performed on RNA extracted from the cutaneous and mucosal epithelium at 0 hour, 12 hours, 1 day, 3 days, and 5 days following injury, as well as unwounded control tissue. Multiple biological replicates (4 to 6 biological replicates) were measured at each condition. A custom Agilent 4x44K rabbit microarray was utilized.

2010-12-01 | E-GEOD-25261 | biostudies-arrayexpress

Pharmacological YAP activation promotes regenerative repair of cutaneous wounds.

Project description:Chronic cutaneous wounds remain a persistent unmet medical need that decrease expectancy and quality of life. Here, we report that topical application of PY-60, a small molecule activator of the transcriptional coactivator YAP, promotes regenerative repair of cutaneous wounds in pig and human models. Pharmacological YAP activation enacts a reversible pro-proliferative transcriptional program in keratinocytes and dermal cells that results in accelerated re-epithelization and regranulation of the wound bed. These results demonstrate that transient topical administration of a YAP activating agent may represent a generalizable therapeutic approach to treating chronic wounds.

2023-06-11 | GSE234332 | GEO

Gene expression profiles of Calu-3 lung epithelial cells after neutrophil transmigration

Project description:Injury to the epithelium is integral to the pathogenesis of many inflammatory lung diseases, and epithelial repair is a critical determinant of clinical outcome. However, the signaling pathways regulating such repair are incompletely understood. Herein, we used in vitro and in vivo models to define these pathways. Human neutrophils were induced to transmigrate across monolayers of human lung epithelial cells in the physiologic basolateral-to-apical direction to a gradient of fMLP. Control wells were treated with fMLP alone. Indicated wells were pretreated with an anti-CD47 blocking antibody, which exacerbates epithelial injury. This allowed study of the neutrophil contribution not only to the initial epithelial injury, but also to its repair, as manifest by restoration of transepithelial resistance (TER) and re-epithelialization of the denuded epithelium. Microarray analysis of epithelial gene expression revealed that neutrophil transmigration activated β-catenin signaling, and this was verified by real time PCR, nuclear translocation of β-catenin, and TOPFlash reporter activity. This pathway represents a potential therapeutic target to accelerate physiologic recovery in inflammatory lung diseases. Total of 20 samples: Calu-3 cells that were untreated, treated with fMLP, treated with fMLP and neutrophil transmigration, and treated with anti-CD47 antibodies, fMLP, and neutrophil transmigration; cDNA was pooled from n=3 experiments; No biological replicates

2011-08-27 | E-GEOD-31697 | biostudies-arrayexpress

Identification of a myofibroblast-specific expression signature in skin wounds

Project description:After skin injury fibroblasts migrate into the wound and transform into contractile extracellular matrix-producing myofibroblasts to promote skin repair. Persistent activation of myofibroblasts can cause excessive fibrotic reactions, but the underlying mechanisms are not fully understood. We used SMA-GFP transgenic mice to study myofibroblast recruitment and activation in skin wounds. Myofibroblasts were initially recruited to wounds three days post injury reached a maximum after seven days and subsequently declined. Expression profiling showed that 1749 genes were differentially expressed in sorted myofibroblasts from wounds seven days post injury. GO-Term analysis associated most of these genes with the extracellular region and cell periphery including upregulated genes encoding for ECM proteins, integrins and focal adhesion proteins and a specific set of growth factors, cytokines and chemokines promoting the healing response. In contrast, cell adhesion molecules involved in cell-cell interaction were downregulated. Novel genes not yet known to be expressed in myofibroblast were found. Hence, this first characterization of a myofibroblast specific expression network at the peak of granulation tissue formation in situ provides important insights into myofibroblast activation in skin wounds and identifies novel target genes to control excessive ECM deposition during fibrotic reactions.

2017-12-30 | GSE95786 | GEO

Thrombospondin-4 is a soluble dermal signal that selectively promotes fibroblast migration and keratinocyte proliferation for skin regeneration and wound healing

Project description:Thrombosponin-4 (THBS4) is a non-structural extracellular matrix molecule associated with tissue regeneration and a variety of pathological processes characterized by increased cell proliferation and migration. However, the mechanisms of how THBS4 regulates cell behaviour as well as the pathways contributing to its effects have remained largely unexplored. In the present study we investigated the role of THBS4 in skin regeneration both in vitro and in vivo. We found that THBS4 expression was upregulated in the dermal compartment of healing skin wounds in humans as well as in mice. Application of recombinand THBS4 protein promoted cutaneous wound healing in mice and selectively stimulated migration of primary fibroblasts as well as proliferation of keratinocytes in vitro. By using a combined proteotranstriptomic pathway analysis approach we discovered that beta-catenin acted as a hub for THBS4-dependent cell signaling and likely plays a key role in promoting its downstream effects. Out results suggest that THBS4 is an important contributor to wound healing and its incorporation into novel wound healing therapies may be a promising strategy for treatment of hard-to-heal wounds.

2022-02-17 | PXD027364 | Pride

Transcription profiling of mouse conditional knock out of beta-catenin by K19-CRE at E7.5

Project description:expression profile of conditional knock out of beta-catenin by K19-CRE at E7.5. Tested a wild type with two alleles of beta-catenin, a heterzyote with one deleted allele and the conditional null in the domain on cytokeratin 19 driven CRE expression

2008-06-12 | E-GEOD-2519 | biostudies-arrayexpress

Inflammatory proteins and neutrophil extracellular traps increase in burn blister fluid after 24 hours post-burn

Project description:Burn wound blister fluid is a valuable matrix for understanding the biological pathways associated with burn injury. In this study, 152 blister fluid samples collected from paediatric burn wounds at two different hospitals were analysed using mass spectrometry proteomic techniques. The protein abundance profile at different days post-burn indicated that there were more proteins associated with cellular damage/repair in the first 24 hours, whereas after this point there were more proteins associated with antimicrobial defence and inflammation. The inflammatory proteins persisted at a high level in the blister fluid for more than 7 days. This may indicate that removal of burn blisters prior to two days post-burn is optimal to prevent excessive or prolonged inflammation in the wound environment. Additionally, many proteins associated with the neutrophil extracellular trap (NET) pathway were increased post-burn, further implicating NETs in the post-burn inflammatory response. NET inhibitors may therefore be a potential treatment to reduce post-burn inflammation and coagulation pathology and enhance burn wound healing outcomes.

2024-03-04 | PXD050003 | Pride

HOXA3 expression in wound tissue

Project description:To investigate how HOXA3 expression in wound tissue alters gene expression to control selective recruitment of bone marrow-derived cell populations, we utilized murine whole genome expression arrays (MEEBO arrays) to identify differentially expressed genes in cutaneous wounds from db/db (diabetic) mice treated with either CMV-HOXA3 or control plasmid. In addition to unwounded control skin, we chose day 4 as the time point to harvest the wounds for RNA isolation, which represents the transition from inflammatory to proliferative phase of wound repair, and precedes the observed differences in BMDC mobilization and recruitment at day 7. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Disease State: cutaneous wound/control skin unwounded skin, wounded skin treated with control plasmid, wounded skin treated with HOXA3

2009-10-12 | E-GEOD-13324 | biostudies-arrayexpress

A novel epidermal-specific role for arginase1 during cutaneous wound repair

Project description:Non-healing wounds are a major area of unmet clinical need that remain problematic to treat; therefore, improved understanding of pro-healing mechanisms is invaluable. The enzyme arginase1 is involved in pro-healing responses with its role in macrophages best-characterised. Arginase1 is also expressed by keratinocytes; however, the function of arginase1 in these critical wound repair cells is not understood. We characterised arginase1 expression in keratinocytes during normal cutaneous repair and reveal de novo temporal and spatial expression at the epidermal wound edge. Interestingly, epidermal arginase1 expression was decreased in both human and murine delayed healing wounds. We, therefore, generated a keratinocyte specific arginase1-null mouse model (K14-cre;Arg1fl/fl) to explore arginase function. Wound repair, linked to changes in keratinocyte proliferation, migration and differentiation, was significantly delayed in K14-cre;Arg1fl/flmice. Gene expression was studied by microarray.

2021-07-07 | E-MTAB-10213 | biostudies-arrayexpress

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