Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Single-Cell RNA-Seq analysis of diabetic wound CD45+ cells in STZ-induced mice

ABSTRACT: The crucial role of immune cells in the healing of chronic diabetic wounds is widely known, but previous in vitro classification and marker genes of immune cells may not be fully applicable to cells in the microenvironment of chronic wounds. The heterogeneity of immune cells was studied and classified at the single-cell level in a chronic wound model. We performed single-cell sequencing of CD45+ immune cells within the wound edge and obtained 17 clusters of cells, including 4 clusters of macrophages. This project has provided an important reference for the study of immune-related mechanisms in diabetic chronic wounds.

ORGANISM(S): Mus musculus

PROVIDER: GSE186821 | GEO | 2023/01/17

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Angiogenin Released from ABCB5+ Stromal Precursors Improves Healing of Diabetic Wounds by Promoting Angiogenesis

Project description:Severe angiopathy is a major driver for diabetes associated secondary complications. Knowledge on underlying mechanisms essential for advanced therapies to attenuate these pathologies is limited. Injection of ABCB5+ stromal precursors (SPs) at the edge of non-healing diabetic wounds in a murine db/db model, closely mirroring human type II diabetes, profoundly accelerates wound closure. Strikingly, enhanced angiogenesis was substantially enforced by the release of the ribonuclease angiogenin from ABCB5+ SPs. This compensates for the profoundly reduced angiogenin expression in non-treated murine and human chronic diabetic wounds. Silencing of angiogenin in ABCB5+ SPs prior to injection significantly reduced angiogenesis, reduced numbers of M2 macrophages and delayed wound closure in diabetic db/db mice implying an unprecedented key role for angiogenin in tissue regeneration in diabetes. These data hold significant promise for further refining SPs-based therapies of non-healing diabetic foot ulcers and other pathologies with impaired angiogenesis.

2021-08-12 | GSE181881 | GEO

Wound healing and hair follicle regeneration with topical BRAF inhibitor therapy in a diabetic model

Project description:Wound healing is a multi-step process to rapidly restore barrier function. This process is often impaired in diabetic patients resulting in chronic wounds and amputation. We previously found that paradoxical activation of the mitogen-activated protein kinase (MAPK) pathway via topical administration of the BRAF inhibitor vemurafenib accelerates wound healing by activating keratinocyte proliferation and reepithelialization pathways in healthy mice. Herein, we investigated whether this wound healing acceleration also occurs in impaired diabetic wounds and found that topical vemurafenib not only improves wound healing in a murine diabetic wound model, but unexpectedly promotes hair follicle regeneration. Neogenic hair follicles expressing Sox-9, CD34 and K15 were found in wounds of diabetic and non-diabetic mice, and their formation can be prevented by blocking downstream MEK signaling. Thus, topically applied BRAF inhibitors may accelerate wound healing, and promote the restoration of improved skin architecture in both normal and impaired wounds.

2021-05-22 | GSE148037 | GEO

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

Transcriptional programming of human epidermis during wound repair and in pressure ulcer at single-cell resolution

Project description:Pressure ulcer (PU) is a chronic non-healing wound caused by continuous pressure of the bodyweight to the skin, which is often seen in spinal cord injury patients and in the bedridden elderly population. In spite of high mortality, the pathophysiology of PU remains poorly understood. We performed single-cell transcriptomic analysis of epidermal cells from PU wound-edges, and compared them with epidermal cells from the intact skin and normal acute wounds (AW) of healthy donors. We identified four keratinocyte clusters, one melanocyte cluster, and one immune cell cluster, and the cellular heterogeneity and gene expression were altered in PU. Our findings provided a high-resolution map of human PU and AW, which are likely to yield new areas for exploration of the pathophysiology of chronic wounds and development of wound therapy.

2021-03-28 | GSE137897 | GEO

miRNA regulation in diabetes associated impaired wound healing

Project description:Circulating miRNAs constitute a novel class of disease biomarkers, which are altered in diabetes but the effect of diabetes associated inflammation as seen in chronic wounds is unknown. We here compared the miRNA pattern in diabetic patients in presence or absence of chronic wound with PAD. The clinical plasma samples were obtained from Heart and Diabetes centre, NRW and compared for plasma miRNA levels in 2 pools of 17 T2DM+PAD+Wound patients vs 2 pools from 20 T2DM controls

2015-06-09 | E-GEOD-49885 | biostudies-arrayexpress

miRNA regulation in diabetes associated impaired wound healing

2015-06-09 | GSE49885 | GEO

MiR146a-loaded engineered exosomes released from silk fibroin patch promote diabetic wound healing

Project description:Unhealable diabetic wounds need to be addressed with the help of newer, more efficacious strategies. Exosomes combined with biomaterials for sustained delivery of therapeutic agents are expected to bring new hope for chronic wound treatment. Here, the engineered exosomes modified for efficiently loading miR-146a and attaching to silk fibroin patch were demonstrated to promote diabetic wound healing. The transcriptomics analysis suggested anti-inflammatory and regenerative effects with SGM-miR146a-Exo@SFP treatment.

2022-11-19 | GSE217981 | GEO

A global transcriptome analysis of skin wounds of diabetic mice (db/db) treated with miR-132 or control mimics

Project description:MiR-132 is one of the most upregulated miRNAs in human skin wounds at the inflammatory phase of healing. MiR-132 inhibits inflammation but promotes growth of epidermal keratinocytes, indicating that it may facilitate the inflammatory-proliferative phase transition during wound repair. Following this line of research, here we evaluated the therapeutic potential of miR-132 in chronic wound using mouse in vivo wound model. We performed a global transcriptome analysis of skin wounds of leptin receptor-deficient (db/db) mice treated with miR-132 or control mimics. Db/db mouse has been used as a type 2 diabetic model with impaired wound healing capacity.

2017-02-01 | GSE92409 | GEO

Heparan sulfate in skin wounds

Project description:Standardized skin wounds were established surgically on mice and allowed to heal during a 15-day period. Expression of genes related to heparan sulfate biosynthesis was studied in wound bed and edges during the healing process. Total RNA was isolated from wound edge (regenerating skin) and wound bed at 2, 6 and 15 days post wounding, as well as from intact control skin. Three animals were used for each time point.

2010-05-22 | E-GEOD-7435 | biostudies-arrayexpress

Acetylation State of Histone Core Defines Macrophage Dynamics in Diabetic Wounds

Project description:Dysregulation of macrophage populations at the wound site is responsible for the non-healing state of chronic wounds. The molecular mechanisms underlying macrophage dysfunction and its control in diabetes are largely unexplored on an epigenetic level. Here, we report that acetyl histone-H3 (Lys27), an epigenetic mark regulating the macrophage transcriptome, is lost in the hostile tissue microenvironment in diabetes. The diabetic microenvironment, profoundly suppresses the acetylation of histone by activating HDACs-dependent deacetylation pathways. This, in consequence, suppress the STAT1 signaling in macrophages maintained in diabetic conditions. Interestingly, the HDAC inhibitor butyrate - via restoring the acetyl histone-H3 (Lys27)-dependent transcriptome - effectively rescues macrophage functions in a diabetic microenvironment. Butyrate reinstalls the STAT1 mediated transcription program and consequently macrophage activity depicting a unique fingerprint of tissue regeneration and inflammation control even in a hostile diabetic microenvironment. Most interesting, butyrate breaks the vicious cycle of inflammation in diabetic wounds. Our study offers novel pathogenic insight and the unique opportunity to reverse perturbed macrophage function thus holding promise to successfully treat diabetic and other chronic wounds and conditions of unrestrained inflammation.

2021-09-14 | GSE183965 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data