Expression data from human keratinocytes after scratch wounds in vitro
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PROVIDER: PRJNA544190 | ENA |
REPOSITORIES: ENA
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Project description:In skin homeostasis, dermal fibroblasts are responsible for coordinating the migration and differentiation of overlying epithelial keratinocytes. As hairy skin heals faster than non-hairy skin, we hypothesised that follicular fibroblasts would accelerate skin re-epithelialisation after injury faster than interfollicular fibroblasts. We found that hair follicle dermal papilla fibroblast conditioned media (DPFi CM) could significantly accelerate wound closure compared to controls partly due to the presence of sAXL in this media. We used microarrays to identify upregulated and downregulated genes in human epidermal keratinocytes incubated with sAXL, DPFi CM and Epilife (keratinocyte growth media;control) after scratch wounds in vitro.
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Project description:Human epidermal keratinocytes undergo tightly controlled program of cell differentiation, leading to the formation of cornified envelope. Primary keratinocytes in vitro, under calcium stimulation mimic the differentiation program observed in vivo. Analysis of the transcription profile of two cell population, such as proliferating cells and differentiating cells helps to discover new genes implicated in that process and to understand the mechanisms of regulation of the keratinocyte differentiation. Primary human keratinocytes were cultured under proliferating (Day 0, sub-confluent cells) and differentiating (seven days of high calcium medium) conditions. As a source of cells, we used normal skin from different body sites: back, foreskin, palmoplantar. RNA extracted from cultured primary human keratinocytes were isolated from five different donors. We compared the expression profiles of proliferating versus differentiating keratinocytes.
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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.
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Project description:Covering denuded dermal surface after injury requires migration, proliferation and differentiation of skin keratinocytes. To clarify the major traits controlling these intermingled biological events, we surveyed the genomic modifications occurring during the course of a scratch closure of cultured human keratinocytes. Using a DNA microarray approach, we report the identification of 161 new markers of epidermal repair. Expression data, combined with functional analysis performed with specific inhibitors of ERK, p38[MAPK] and PI3 kinases, demonstrate that kinase pathways exert very selective functions by precisely controlling the expression of specific genes. Inhibition of the ERK pathway totally blocks the wound closure and inactivates many early transcription factors and EGF-type growth factors. P38[MAPK] inhibition only delays “healing”, probably in line with the control of genes involved in the propagation of injury-initiated signalling. In contrast, PI3 kinase inhibition accelerates the scratch closure and potentiates the scratch-dependent stimulation of three genes related to epithelial cell transformation, namely HAS3, HBEGF and Ets1. Our results define in vitro human keratinocyte wound closure as a reparation process resulting from a fine balance between positive signals controlled by ERK and p38[MAPK], and negative ones triggered off by PI3 kinase. The perturbation of any of these pathways might lead to dysfunction in the healing process, as those observed in pathological wounding phenotypes, such as hypertrophic scars or keloids. Keywords: Transcriptome of healing keratinocytes
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Project description:Patients with recessive dystrophic epidermolysis bullosa (RDEB) lack functional Type VII collagen and suffer severe blistering and chronic wounds that ultimately lead to infection and development of lethal squamous cell carcinoma (SCC). The discovery of induced pluripotent stem cells (iPSCs) and the ability to edit the genome bring the possibility to provide definitive genetic therapy through corrected autologous tissues. We have formed a multidisciplinary team with the ultimate goal to develop an iPSC-based therapy for RDEB. Here, we present a clinical protocol that generates autologous, corrected epithelial keratinocyte sheets with the COL7A1 gene mutation corrected for grafting on to patients. We demonstrate the utility of sequential reprogramming and novel adenovirus-associated viral genome editing to generate corrected iPSC banks. iPSC-derived keratinocytes were produced with minimal heterogeneity and secreted wild-type collagen VII, resulting in stratified epidermis in vitro and in vivo in mice. Sequencing of corrected cell lines prior to tissue formation revealed heterogeneity of SCC-predisposing mutations, allowing us to select COL7A1 corrected banks with minimal mutational burden for downstream epidermis production. Our results provide a first clinical platform to use iPSCs in the treatment of debilitating genodermatoses. Microarray analysis of iPS-derived keratinocytes from two RDEB patients (iPS-K1 and iPS-K3), corresponding patient keratinocytes (AHK1 and AHK2), normal human keratinocytes (NHK), as well as H9 human embryonic stem cells (hESC - H9). All samples were analyzed in duplicate and differential gene expression was measured relative to H9.
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