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

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

PROVIDER: PRJNA509935 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8316300.fastq.gz	Fastqsanger.gz
	SRR8316310.fastq.gz	Fastqsanger.gz
	SRR8316301.fastq.gz	Fastqsanger.gz
	SRR8316311.fastq.gz	Fastqsanger.gz
	SRR8316302.fastq.gz	Fastqsanger.gz

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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

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

Project description:Defective cell migration causes delayed wound healing (WH) and chronic skin lesions. Autologous micrograft (AMG) therapies have recently emerged as a new effective and affordable treatment able to improve wound healing capacity. However, the precise molecular mechanism through which AMG exhibits its beneficial effects remains unrevealed. Herein we show that AMG improves skin re-epithelialization by accelerating the migration of fibroblasts and keratinocytes. More specifically, AMG-treated wounds showed improvement of indispensable events associated with successful wound healing such as granulation tissue formation, organized collagen content, and newly formed blood vessels. We demonstrate that AMG is enriched with a pool of WH-associated growth factors that may provide the starting signal for a faster endogenous wound healing response. This work links the increased cell migration rate to the activation of the extracellular signal-regulated kinase (ERK) signaling pathway, which is followed by an increase in matrix metalloproteinase expression and their extracellular enzymatic activity. Overall we reveal the AMG-mediated wound healing transcriptional signature and shed light on the AMG molecular mechanism supporting its potential to trigger a highly improved wound healing process. In this way, we present a framework for future improvements in AMG therapy for skin tissue regeneration applications.

| S-EPMC7206041 | biostudies-literature

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

Clearance of p21-highly-expressing senescent cells accelerates wound healing

Project description:Clearance of p21-highly-expressing senescent cells accelerates wound healing

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ANT2 accelerates cutaneous wound healing in aged skin by reverse senescence

Project description:ANT2 accelerates cutaneous wound healing in aged skin by reverse senescence

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Clearance of p21-highly-expressing senescent cells accelerates cutaneous wound healing

Project description:Clearance of p21-highly-expressing senescent cells accelerates cutaneous wound healing

| PRJNA1167732 | ENA

Clearance of p21-highly-expressing senescent cells accelerates wound healing

Project description:Targeting senescent cells for therapeutic purposes is gaining momentum across various organ systems. However, concerns about potential off-target effects have been raised. Previous studies have shown that removing senescent cells expressing high levels of p16 (p16high) can hinder processes like wound healing. Here, we identify a distinct senescent cell population during dermal wound healing characterized by high expression level of p21 (p21high) using the p21-Cre mouse model. Using a standard cutaneous injury model, we find that eliminating p21high cells can expedite wound closure, in contrast to the effects of removing p16high cells. Through Xenium, a single cell spatial imaging platform, we show that p21high cells are distinct from p16high cells, with p21high cells mainly comprising fibroblasts, immune cells, keratinocytes, and endothelial cells with a pro-inflammatory profile. Moreover, inhibition of NF-kB signaling specifically from p21high cells partially contributes to the accelerated wound healing rates. These findings highlight the heterogeneity of senescent cells during wound healing responses within the skin and likely in other conditions.

2024-10-07 | GSE278611 | GEO

ANT2 accelerates cutaneous wound healing in aged skin by reverse senescence

Project description:An effective healing response is critical to healthy aging. Thus, the connection of regeneration and aging is needed to understand the complicated age-related healing process. Energy metabolism has been a common hallmark of both studies. In recent years, it become an emerging factor of skin homeostasis. Adenine nucleotide translocase-2 (ANT2) is a known cell proliferation marker and mediator of ATP import into mitochondria for energy homeostasis. Although energy homeostasis and the maintenance of mitochondrial function are critical for wound healing, the role of ANT2 in wound healing has not been elucidated. We found that ANT2 expression decreased during aging in mouse skin as well as during cellular senescence. Interestingly, overexpression of ANT2 in aged mouse skin promoted the healing of full-thickness cutaneous wounds. In addition, upregulation of ANT2 in replicative senescent human diploid dermal fibroblasts (HDFs) induced cell proliferation and migration, which are critical for the wound healing process. Furthermore, overexpression of ANT2 increased ATP production rate by activating the glycolysis pathway and also increased mitophagy, both of which are involved in energy homeostasis. Notably, ANT2-mediated upregulation of HSPA6 in aged HDFs inhibited the expression of pro-inflammatory genes that mediate cellular senescence and mitochondrial damage. This study demonstrates a new physiological role of ANT2 in skin wound healing via regulation of cell proliferation, energy homeostasis, and inflammation. Thus, our study links energy metabolism to skin homeostasis and identifies a genetic factor for improving wound healing with aging model.

2022-11-21 | GSE206141 | GEO

Clearance of p21-highly-expressing senescent cells accelerates cutaneous wound healing

2024-10-01 | GSE278527 | GEO

Damaged Brain Accelerates Bone Healing by Releasing Exosomes that Target Osteoprogenitors

Project description:Clinical evidence has established that concomitant traumatic brain injury accelerates bone healing, but the underlying mechanism is unclear. This study showed that after TBI, injured neurons, mainly those in the hippocampus, released osteogenic microRNA (miRNA)-enriched exosomes, which targeted osteoprogenitors in bone to stimulate bone formation. Importantly, increased fibronectin expression on exosomal surface contributed to targeting of osteoprogenitors in bone by TBI exosomes, thereby implying that modification of the exosome surface fibronectin could be used in bone-targeted drug delivery. Together, our findings have established a novel role of central regulation in bone formation and a clear link between injured neurons and osteogenitors, both in animals and clinical settings.

2021-07-13 | PXD022126 | Pride

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