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Human Skin Transcriptome during Epidermal Wound Healing

ABSTRACT: In order to clarify the human response of re-epithelialization, we biopsied split-thickness skin graft donor site wounds immediately before and after harvesting, as well as during the healing process 3 and 7 days thereafter. Altogether 25 biopsies from 8 patients qualified for the study. All samples were analysed by genome-wide microarrays. Here we identified the genes associated with normal skin re-epithelialization on time-scale, and organized them by similarities according to their induction or suppression patterns during wound healing.

ORGANISM(S): Homo sapiens

PROVIDER: GSE28914 | GEO | 2011/04/29

SECONDARY ACCESSION(S): PRJNA140567

REPOSITORIES: GEO

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Human Skin Transcriptome during Epidermal Wound Healing

Project description:In order to clarify the human response of re-epithelialization, we biopsied split-thickness skin graft donor site wounds immediately before and after harvesting, as well as during the healing process 3 and 7 days thereafter. Altogether 25 biopsies from 8 patients qualified for the study. All samples were analysed by genome-wide microarrays. Here we identified the genes associated with normal skin re-epithelialization on time-scale, and organized them by similarities according to their induction or suppression patterns during wound healing. Overall 25 samples were analyzed

2011-04-29 | E-GEOD-28914 | biostudies-arrayexpress

Gene expression profiling of negative-pressure-treated split-thickness skin graft donor site wounds reveals novel effects on epithelialization

Project description:Negative-pressure wound therapy (NPWT) is widely used to improve skin wound healing and to accelerate wound bed preparation. Although NPWT has been extensively studied as a treatment for deep wounds, its effect on epithelialization of superficial dermal wounds remains unclear. To clarify the effect of NPWT on reepithelialization, we applied NPWT on split- thickness skin graft donor sites from the first postoperative day (POD) to the seventh POD. Six patients took part in the study and two samples were obtained from each. The first biopsy sample was taken at elective surgery before split-thickness skin grafting and the second one during reepithelialization on the seventh POD. In all 12 samples (eight from four NPWT patients, and four from two control patients) were collected for this study. From each sample, we carried out a comprehensive genome-wide microarray analysis. Data from patients receiving NPWT were compared groupwise with data from those not receiving NPWT. Overall 12 samples were analyzed

2011-10-24 | E-GEOD-33169 | biostudies-arrayexpress

Alcaligenes faecalis corrects aberrant matrix metalloproteinase expression to promote re-epithelialization of diabetic wounds

Project description:Chronic wounds are a common and costly complication of diabetes, where multifactorial defects contribute to dysregulated skin repair, inflammation, tissue damage, and infection. We previously showed that aspects of the diabetic foot ulcer microbiota were correlated with poor healing outcomes, but many microbial species recovered remain uninvestigated with respect to wound healing. Here we focused onAlcaligenes faecalis, a Gram-negative bacterium that is frequently recovered from chronic wounds but rarely causes infection. Treatment of diabetic wounds withA. faecalisaccelerated healing during early stages. We investigated the underlying mechanisms and found thatA. faecalistreatment promotes re-epithelialization of diabetic keratinocytes, a process which is necessary for healing but deficient in chronic wounds. Overexpression of matrix metalloproteinases in diabetes contributes to failed epithelialization, and we found thatA. faecalistreatment balances this overexpression to allow proper healing. This work uncovers a mechanism of bacterial-driven wound repair and provides a foundation for the development of microbiota-based wound interventions.

2024-03-30 | GSE261418 | GEO

Novel epoxy-tiglianes stimulate keratinocyte wound healing responses and re-epithelialization via protein kinase C activation

Project description:Impaired re-epithelialization is a hallmark of non-healing, chronic skin wounds. These represent major causes of patient morbidity, particularly amongst ever-increasing ageing and diabetic populations, posing significant challenges to healthcare providers worldwide. Despite many treatment options being available, these often offer limited benefits to healing outcomes. We address the need for more efficacious treatments through evaluation of novel epoxy-tigliane compounds as chronic wound pharmaceuticals, based on their effectiveness in promoting keratinocyte healing responses and re-epithelialization in vivo. Here, we identify that prototype epoxy-tigliane (EBC-46) and analogue (EBC-211), accelerate G1/S and S/G2 cell cycle transitions and proliferation in a normal human keratinocyte cell line of skin origin (HaCaTs). EBC-46 and EBC-211 further induce HaCaT migration/wound repopulation, even with mitomycin C treatment, suggesting epoxy-tiglianes can promote migration/repopulation independently of proliferation. Epoxy-tiglianes modulate keratin, DNA synthesis/replication, cell cycle/proliferation, motility/migration, differentiation, proteinase; and cytokine/chemokine gene expression, to facilitate enhanced responses. Although epoxy-tiglianes down-regulate cytokine/chemokine agonists of keratinocyte proliferation/migration, we demonstrate that enhanced HaCaT responses are mediated through protein kinase C (PKC) phosphorylation and abrogated by inhibition of PKC activation with bisindolylmaleimide-1 (BIM-1). By identifying how epoxy-tiglianes stimulate keratinocyte healing responses, we highlight their potential as novel therapeutics for impaired re-epithelialization associated with non-healing, chronic wounds.

2019-08-01 | GSE122297 | GEO

Gene expression profiling of negative-pressure-treated split-thickness skin graft donor site wounds reveals novel effects on epithelialization

2011-10-25 | GSE33169 | GEO

Menstrual fluid factors facilitate tissue repair: Identification and functional action in endometrial and skin repair

Project description:Repair after damage is essential for tissue homeostasis. Post-menstrual repair of the uterine endometrium is a unique cyclical manifestation of rapid, scar-free, tissue repair taking ~3-5 days. Skin repair post-wounding is slower (~2 weeks) and, in the case of chronic wounds, takes months/years to restore integrity. Herein, the unique ‘rapid-repair’ endometrial environment is translated to the ‘slower-repair’ skin environment. Menstrual fluid (MF), the milieu of post-menstrual endometrial repair, facilitates healing of endometrial and keratinocyte ‘wounds’ in vitro, promoting cellular adhesion and migration, stimulates keratinocyte migration in an ex vivo human skin-reconstruct model and promotes re-epithelialization in an in vivo porcine wound model. Proteomic analysis of MF identified a large number of proteins; several proteins were selected for further investigation, with the endometrium demonstrated as the source of these factors. Functionally, they promote repair of endometrial and keratinocyte wounds by promoting migration, differing significantly from currently available wound-repair treatments, which mainly promote proliferation. Development of these and other menstrual fluid factors into a ‘migration-inducing’ treatment paradigm will provide novel therapies for tissue repair.

2018-07-30 | PXD007234 | Pride

Setd2 Epidermal Deficiency Promotes Cutaneous Wound Healing via Activation of AKT/mTOR Signaling (ChIP-Seq)

Project description:Skin wound healing is one of the major prevalent medical problems in the worldwide. Wound healing involves multi-process synergy and re-epithelialization is an essential part of wound healing. Histone H3K36 tri-methylase Setd2 has been extensively studied in different biological processes and diseases. However, the function of Setd2 in the wound healing remains unclear. To elucidate the biological role of Setd2 in the skin wound healing, conditional gene targeting was employed to establish epidermis-specific Setd2-deficient mice. We found that Setd2 deficiency resulted in accelerated re-epithelialization during cutaneous wound healing by promoting keratinocytes proliferation and migration. Furthermore, we demonstrated that loss of Setd2 activated the AKT/mTOR pathway, and pharmacological inhibitions of AKT and mTOR with MK2206 and rapamycin delayed wound closure, respectively. In conclusion, our results reveal the essential role of Setd2 in skin wound healing that is Setd2 loss promotes cutaneous wound healing via activation of AKT/mTOR signaling.

2020-12-25 | GSE163858 | GEO

Setd2 Epidermal Deficiency Promotes Cutaneous Wound Healing via Activation of AKT/mTOR Signaling (RNA-Seq)

2020-12-25 | GSE163860 | GEO

Characterization of wound healing in Atlantic salmon (Salmo salar) post-smolt, and the effect of stress on the healing process

Project description:The aim of this study was to assess the effect induced by high fish density on cutaneous wound healing in post-smolt Atlantic salmon. Our findings suggest that high fish density enhances inflammation and represses cell proliferation, tissue secretion and collagen synthesis in the healing wounds. These processes are further manifested in the different layers of the skin, such as delayed re-epithelialization, altered mucus response, reduced scale mineralization, enhanced wound pigmentation and delayed organization of dense connective tissue. Temporarily changes in wound healing mechanisms result in permanent differences in wound contraction. In conclusion, our results show that high fish density dispose the fish for an enhanced immune response and delayed tissue repair, which ultimately results in delayed wound healing.

2018-11-06 | GSE122142 | GEO

Autologous microgratf accelerates endogenous wound healing response through ERK-induced cell migration.

Project description:Defective fibroblast migration cause delayed wound healing (WH) and chronic skin lesions. Autologous micrograft (AMG) therapies have recently emerged as a new effective treatment able to improve wound healing capacity. However, the molecular mechanisms connecting their beneficial outcomes with the wound healing process are still unrevealed. Here, we show that AMG modulates primary fibroblast migration and accelerates skin re-epithelialization without affecting cell proliferation. We demonstrate that AMG is enriched in a pool of WH-associated growth factors that may provide the initiation signal for faster endogenous wound healing response. This, in turn leads to increased cell migration rate by elevating activity of ERK and subsequent activation of matrix metalloproteinase expression and their extracellular enzymatic activity. Moreover, AMG-treated wounds showed increased granulation tissue formation and organized collagen content. Overall, we shed light on AMG molecular mechanism supporting its potential to trigger highly improved wound healing process.

2020-01-01 | GSE123829 | GEO

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