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Fibroblast Growth Factor-2 bound to specific dermal fibroblasts-derived extracellular vesicles is protected from degradation: relevance to wound healing

ABSTRACT: Fibroblast Growth Factor-2 bound to specific dermal fibroblasts-derived extracellular vesicles is protected from degradation: relevance to wound healing

PROVIDER: PRJNA877679 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21469160_1.fastq.gz	Fastqsanger.gz
	SRR21469160_2.fastq.gz	Fastqsanger.gz
	SRR21469161_1.fastq.gz	Fastqsanger.gz
	SRR21469161_2.fastq.gz	Fastqsanger.gz
	SRR21469162_1.fastq.gz	Fastqsanger.gz

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Fibroblast Growth Factor-2 bound to specific dermal fibroblasts-derived extracellular vesicles is protected from degradation: relevance to wound healing

Project description:Fibroblast growth factor-2 (FGF2) has multiples roles in cutaneous wound healing but its natural low stability prevents the development of its use in therapeutic for impaired skin repair. Here we show that FGF2 binds the outer surface of dermal fibroblast (DF)-derived extracellular vesicles (EVs) and this association protects FGF2 from fast degradation. We performed RNA-seq analysis after EV treatment to examine modulated genes in DFs.

2022-12-21 | GSE212873 | GEO

Dynamic Single Cell Proteomics Reveals the Functional Shifts of Dermal Sheath Cells during Wound Healing

Project description:Single-cell proteomics data of dermal sheath cells (DSCs) during wound healing, generated using SCoPE2-MS, highlighting dynamic protein expression and functional changes across different healing stages.

2024-10-28 | PXD057239 |

Hypoxia and Foxn1 alter dermal fibroblasts proteomics signature to redirect scar-less to scar-forming skin wound healing in Foxn1-/- mice

Project description:Hypoxia is one of the factors that govern reparative vs regenerative skin wound healing. Data-independent acquisition (DIA) experiment was carried out to study the effect of hypoxia and Foxn1 on mice dermal fibroblast proteomics signature and skin wound healing of Foxn1-deficient (Foxn1-/-) mice.

2024-06-20 | PXD041939 | Pride

Thrombospondin-4 is a soluble dermal signal that selectively promotes fibroblast migration and keratinocyte proliferation for skin regeneration and wound healing

Project description:Thrombosponin-4 (THBS4) is a non-structural extracellular matrix molecule associated with tissue regeneration and a variety of pathological processes characterized by increased cell proliferation and migration. However, the mechanisms of how THBS4 regulates cell behaviour as well as the pathways contributing to its effects have remained largely unexplored. In the present study we investigated the role of THBS4 in skin regeneration both in vitro and in vivo. We found that THBS4 expression was upregulated in the dermal compartment of healing skin wounds in humans as well as in mice. Application of recombinand THBS4 protein promoted cutaneous wound healing in mice and selectively stimulated migration of primary fibroblasts as well as proliferation of keratinocytes in vitro. By using a combined proteotranstriptomic pathway analysis approach we discovered that beta-catenin acted as a hub for THBS4-dependent cell signaling and likely plays a key role in promoting its downstream effects. Out results suggest that THBS4 is an important contributor to wound healing and its incorporation into novel wound healing therapies may be a promising strategy for treatment of hard-to-heal wounds.

2022-02-17 | PXD027364 | Pride

Characterizing dermal transcriptional change in the progression from sun-protected skin to actinic keratosis. II[

Project description:Here we used a pan-cytokeratin antibody to differentiate the epidermal from dermal compartment and assayed over 18,000 RNA probes from multiple regions of interest (ROI) comparing sun protected skin, and two regions (edge and center) from AK/sun damaged skin. This allows for a trajectory from sun protected to sun damaged within an individual. Traditionally, cancer biology focusses on change within the tumor compartment for diagnosis and staging and current genetic profiling of actinic keratosis (the precursor lesion for cutaneous squamous cell carcinoma) has focused on analysis limited to whole skin or the epidermal compartment alone. Here we use spatial transcriptomics to compare and contrast the epidermal and stromal compartments from different regions of actinic keratosis and matched sun protected skin from six individuals. Our data show that the major changes in AK at the transcriptional level are evident in the dermal compartment. Sun protected skin (n=5-6 from 6 individuals for a total of 34 ROI), the center of an AK lesion (n=3 for a total of 18 ROI) and edge of the AK lesion (n=2-3 for a total of 17 ROI) representing sun-damaged skin, from six unrelated individuals, the center of an AK lesion (n=3 for a total of 18 ROI) and edge of the AK lesion (n=2-3 for a total of 17 ROI) representing sun-damaged skin, from six unrelated individuals.

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Characterizing dermal transcriptional change in the progression from sun-protected skin to actinic keratosis. [I]

2022-12-19 | GSE220998 | GEO

Olfactomedin-4 improves cutaneous wound healing by promoting skin cell proliferation and migration

Project description:Olfactomedin-4 (OLFM4) is an olfactomedin-domain-containing glycoprotein which regulates cell adhesion, proliferation, gastrointestinal inflammation, innate immunity and cancer metastasis. In the present study investigated its role in skin regeneration and wound healing. We found that OLFM4 expression is transiently upregulated in the proliferative phase of cutaneous wound healing in humans as well as in mice. Moreover, a significant increase in OLFM4 expression was detected in the skin of lesional psoriasis, a chronic inflammatory disease characterized by keratinocyte hyperproliferation. In vitro experiments demonstrated that OLFM4 can selectively stimulate keratinocyte proliferation and increase both keratinocyte and fibroblast migration ability. Using proteotransciptomic pathway analysis we revealed that transcription factors POU5F1/OCT4 and ESR1 acted as hubs for OLFM4-dependent signalling in keratinocytes. In vivo experiments utilizing mouse splinted full-thickness cutaneous wound healing model showed that application of recombinant OLFM4 protein can significantly improve wound healing time. Taken together, our results suggest that OLFM4 is a transiently upregulated inflammatory signal that promotes wound healing by supporting the functions of both dermal and epidermal cell compartments.

2022-05-20 | PXD029881 | Pride

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

Distinct Regulatory Programs Control the Latent Regenerative Potential of Dermal Fibroblasts during Wound Healing

Project description:Distinct Regulatory Programs Control the Latent Regenerative Potential of Dermal Fibroblasts during Wound Healing

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

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