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Setd2 Epidermal Deficiency Promotes Cutaneous Wound Healing via Activation of AKT/mTOR Signaling

ABSTRACT: Setd2 Epidermal Deficiency Promotes Cutaneous Wound Healing via Activation of AKT/mTOR Signaling

PROVIDER: PRJNA687765 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13306467_1.fastq.gz	Fastqsanger.gz
	SRR13306467_2.fastq.gz	Fastqsanger.gz
	SRR13306468_1.fastq.gz	Fastqsanger.gz
	SRR13306468_2.fastq.gz	Fastqsanger.gz
	SRR13306469_1.fastq.gz	Fastqsanger.gz

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Setd2 Epidermal Deficiency Promotes Cutaneous Wound Healing via Activation of AKT/mTOR Signaling (RNA-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 | GSE163860 | GEO

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

2020-12-25 | GSE163858 | GEO

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

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

| PRJNA687767 | ENA

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

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

| PRJNA687766 | ENA

SETD2 epidermal deficiency promotes cutaneous wound healing via activation of AKT/mTOR Signalling.

Project description:ObjectivesCutaneous wound healing is one of the major medical problems worldwide. Epigenetic modifiers have been identified as important players in skin development, homeostasis and wound repair. SET domain-containing 2 (SETD2) is the only known histone H3K36 tri-methylase; however, its role in skin wound healing remains unclear.Materials and methodsTo elucidate the biological role of SETD2 in wound healing, conditional gene targeting was used to generate epidermis-specific Setd2-deficient mice. Wound-healing experiments were performed on the backs of mice, and injured skin tissues were collected and analysed by haematoxylin and eosin (H&E) and immunohistochemical staining. In vitro, CCK8 and scratch wound-healing assays were performed on Setd2-knockdown and Setd2-overexpression human immortalized keratinocyte cell line (HaCaT). In addition, RNA-seq and H3K36me3 ChIP-seq analyses were performed to identify the dysregulated genes modulated by SETD2. Finally, the results were validated in functional rescue experiments using AKT and mTOR inhibitors (MK2206 and rapamycin).ResultsEpidermis-specific Setd2-deficient mice were successfully established, and SETD2 deficiency resulted in accelerated re-epithelialization during cutaneous wound healing by promoting keratinocyte proliferation and migration. Furthermore, the loss of SETD2 enhanced the scratch closure and proliferation of keratinocytes in vitro. Mechanistically, the deletion of Setd2 resulted in the activation of AKT/mTOR signalling pathway, while the pharmacological inhibition of AKT and mTOR with MK2206 and rapamycin, respectively, delayed wound closure.ConclusionsOur results showed that SETD2 loss promoted cutaneous wound healing via the activation of AKT/mTOR signalling.

| S-EPMC8168411 | biostudies-literature

Setd2 Epidermal Deficiency Promotes Cutaneous Wound Healing via Activation of AKT/mTOR Signaling

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-12-25 | GSE163861 | GEO

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

Human Oral and Cutaneous Wound Healing Transcriptomes

Project description:Comparative analysis between oral and cutaneous wound healing in humans using paired and sequential biopsies during the repair process.

2018-08-07 | GSE97615 | GEO

SOX2 epidermal overexpression promotes cutaneous wound healing via activation of EGFR/MEK/ERK signaling mediated by EGFR ligands

Project description:We perfomed RNA-seq and wound healing analysis to identify the mechanism how SOX2 promote wound healing. We showed that induction of SOX2 in skin keratinocytes accelerates cutaneous wound healing by promoting keratinocyte migration and proliferation, and enhancement of angiogenesis via the upregulation of EGFR ligands.

2019-09-02 | GSE118859 | GEO

Il-22-Fc in cutaneous wound healing response

Project description:Diabetic foot ulcers (DFU) are one of the major complications in type II diabetes patients and can result in amputation and morbidity. Although multiple approaches are used clinically to help wound closure, many patients still lack adequate treatment. Here we show that IL-20 subfamily cytokines are upregulated during normal wound healing. While there is a redundant role for each individual cytokine in this subfamily in wound healing, mice deficient in IL-22R, the common receptor chain for IL-20, IL-22, and IL-24, display a significant delay in wound healing. Furthermore, IL-20, IL-22 and IL-24 are all able to promote wound healing in type II diabetic db/db mice. When compared to other growth factors such as VEGF and PDGF that accelerate wound healing in this model, IL-22 uniquely induced genes involved in reepithelialization, tissue remodeling and innate host defense mechanisms from wounded skin. Interestingly, IL-22 treatment showed superior efficacy compared to PDGF or VEGF in an infectious diabetic wound model. Taken together, our data suggest that IL-20 subfamily cytokines, particularly IL-20, IL-22, and IL-24, might provide therapeutic benefit for patients with DFU.

2017-03-08 | GSE80419 | GEO

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