The Role of LINGO1 in Epithelial Wound Repair
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA748769 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15210490.fastq.gz | Fastqsanger.gz | |||
| SRR15210491.fastq.gz | Fastqsanger.gz | |||
| SRR15210492.fastq.gz | Fastqsanger.gz | |||
| SRR15210493.fastq.gz | Fastqsanger.gz |
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Project description:Leucine-rich repeat and IgG-like domain containing NOGO-receptor interacting protein 1 (LINGO1) has an inhibitory role in neuronal growth and regeneration following injury; yet LINGO1 involvement in the injury response of other tissues has not been thoroughly explored. Previous studies have demonstrated that the reparative cytokines of the Trefoil factor family interact with members of the LINGO receptor family in maintenance of gastrointestinal barrier integrity, suggesting a role for LINGO receptors in epithelial repair processes. In this study, we investigated whether LINGO1 had a role in alveolar epithelial repair. A mouse alveolar epithelial cell line, MLE-12, was utilized in an in vitro scratch assay as a model of epithelial injury and repair. CRISPR/Cas9-mediated deletion of Lingo1 resulted in significantly reduced wound closure at both 24 and 48 h post-scratch in comparison to parental (WT) cells. We preformed RNA sequencing of 24h post-scratch cells or un-scratched cells, and revealed a set of 147 differentially expressed genes between WT and Lingo1KO cells following scratch.
2024-07-21 | GSE180602 | GEO
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
Project description:Analysis of miRNA expression at different time points of epithelial wound repair of 16HBE14o- cells after mechanical damage of cell monolayer.
2013-10-02 | E-MEXP-3986 | biostudies-arrayexpress
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: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.
2012-07-30 | GSE37947 | GEO
Project description:The mitogen-activated protein kinase kinase (MEK) kinase 1 (MEKK1), also known as MAP3K1, mediates activin B (ActB) signals required for eyelid epithelium morphogenesis during mouse fetal development. The present study investigates the role of MEKK1 in epithelial wound healing, another activin-regulated biological process. In a skin wound model, injury markedly stimulates MEKK1 expression and activity, which are in turn required for the expression of genes involved in extracellular matrix (ECM) homeostasis. MEKK1 ablation or down-regulation by interfering RNA significantly delays skin wound closure and impairs activation of Jun NH2-terminal kinases, induction of plasminogen activator inhibitor (PAI)-1, and restoration of cell-cell junctions of the wounded epidermis. Conversely, expression of wild-type MEKK1 accelerates reepithelialization of full-thickness skin and corneal debridement wounds by mechanisms involving epithelial cell migration, a cell function that is partially abolished by neutralizing antibodies for PAI-1 and metalloproteinase III. Our data suggest that MEKK1 transmits wound signals, leading to the transcriptional activation of genes involved in ECM homeostasis, epithelial cell migration, and wound reepithelialization.
2022-07-13 | GSE201823 | GEO
Project description:Tissue repair processes maintain proper organ function following mechanical or infection related damage. In addition to anti-bacterial properties, MAIT cells express a tissue repair transcriptomic program and promote skin wound healing when expanded. Herein, we use a human‑like full‑thickness skin excision mouse model to assess the underlying mechanisms of MAIT cell tissue repair function. Single-cell RNAseq analysis suggests that skin MAIT cells already express a repair program at steady state. Following skin excision, MAIT cells promote keratinocyte proliferation thereby accelerating healing. Using skin grafts, parabiosis and adoptive transfer experiments, we show that MAIT cells migrate into the wound from other tissues in a TCR independent but CXCR6 dependent manner. Amphiregulin secreted by MAIT cells following excision promotes wound healing. The repair function is independent of sustained TCR stimulation. Overall, our study provides mechanistic insight into MAIT cell wound healing function in the skin.
2023-01-10 | GSE207348 | GEO
Project description:Rationale: Damage to airway epithelium is followed by deposition of extracellular matrix (ECM) and migration of adjacent epithelial cells. We have shown that epithelial cells from asthmatic children fail to heal a wound in vitro. Objectives: To determine whether dysregulated ECM production by the epithelium plays a role in aberrant repair in asthma. Methods: Airway epithelial cells (AEC) from children with asthma (n=36), healthy atopic (n=23) and healthy non-atopic controls (n=53) were investigated by microarray, gene expression and silencing, transcript regulation analysis and ability to close mechanical wounds. Results: Wound repair of AEC from healthy and atopic children were not significantly different and were both faster than AEC from asthmatics. Microarray analysis revealed differential expression of multiple gene sets associated with repair and remodeling in asthmatic AEC. Fibronectin (FN) was the only ECM component whose expression was significantly lower in asthmatic AEC. Expression differences were verified by qPCR and ELISA, and reduced FN expression persisted in asthmatic cells over passage. Silencing of FN expression in non-asthmatic AEC inhibited wound repair, while addition of FN to asthmatic AEC restored reparative capacity. Asthmatic AEC failed to synthesize FN in response to wounding or cytokine/growth factor stimulation. Exposure to 5â, 2âdeoxyazacytidine had no effect on FN expression and subsequent analysis of the FN promoter did not show evidence of DNA methylation. Conclusions: These data show that the reduced capacity of asthmatic epithelial cells to secrete FN is an important contributor to the dysregulated AEC repair observed in these cells. 16 arrays, 2 experimental groups, asthma atopic, AA, and healthy non-atopic, HN.
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Project description:Gas6-Axl signaling drives oral regenerative wound repair
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Project description:Wound healing requires orchestration of cellular migration, adhesion molecule synthesis, and cell cycle regulation. However, the cellular receptors necessary for the repair of damaged tissue remain poorly understood. This study investigated whether extracellular transmembrane receptors in the leucine rich repeat and nogo interacting protein family (LINGO) were required for the recovery of airway epithelial cells from from scratch wound injury. CRISPR/Cas9-mediated deletion mutants for either LINGO1, LINGO2, or LINGO3 or their putative co-receptors, Tumor Necrosis Factor Receptor Superfamily, Member 19 (TROY) and Reticulon 4 Receptor (RTN4R) in the mouse airway epithelial cell line MLE-12 were used for mRNA sequencing. Cells for all lines were grown to a monolayer and subjected to a scratch with a pipette tip. Cells from each mutant line and the parental line were collected for sequencing after 24 hours post-scratch. In addition the parental line was sequenced under baseline un-scratch conditions.
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