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Wound memory of epidermal stem cells [scRNAseq L1-aged]

ABSTRACT: Wound memory of epidermal stem cells [scRNAseq L1-aged]

PROVIDER: PRJNA811146 | ENA |

REPOSITORIES: ENA

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Wound memory of epidermal stem cells [scRNAseq L1 PRT]

Project description:Wound memory of epidermal stem cells [scRNAseq L1 PRT]

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Wound memory of epidermal stem cells [scRNAseq L1-aged]

Project description:Wound priming in epidermal Lrig1 stem cell progeny leads to a more efficient response to future injuries. To understand if primed progenitors maintain during aging the transcriptional program acquired during wound healing in young age, we performed single cell RNA-Seq of Lrig1 stem cell progeny 40 weeks after injury.

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Wound memory of epidermal stem cells [scRNAseq L1 PRT]

Project description:Wound priming in epidermal Lrig1 stem cell progeny leads to a more efficient response to future injuries. To identify a key epigenetic factor of this cellular adaptation, we performed an epigenetic drug screening in Lrig1 genetically labled mice. Pre-treatment with PRT4165 lead to a more efficient wound closure. To understand if PRT4165 was able to recapitulate wound priming, we performed single cell RNA-seq transcriptome profiling of epidermal Lrig1 stem cell progenies from PRT4165-treated or untreated murine skin. [PRT4165is an inhibitor of the enzymatic activity of Ring1a/Ring1b, component of the Polycomb repressive complexes 1 (PRC1), responsible for the monoubiquitination of lysin 119 on histone H2A (H2AK119ub)]

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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.

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