Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Suture-anchored cutaneous tension induces persistent hypertrophic scarring in a novel murine model [miRNA]

ABSTRACT: Hypertrophic scars arise from dysregulated wound healing under prolonged mechanical tension, causing disfiguring fibrosis. However, limited preclinical models replicate key features of human tension-induced scarring. We developed an innovative murine model utilizing suture anchoring to impose persistent transverse-axial stretch across healing incisions, mimicking excessive wound tension that leads to hypertrophy clinically. Dorsal paired incisions were generated in mice, with wound edges on the upper back sutured to the rib cage while leaving wound edges on the lower back relaxed. This localized anchoring restrained wound contraction, maintaining high tension throughout remodeling analogous to scars widening under stress. Stretched upper wounds developed profound fibrotic changes compared to relaxed controls. Scars induced by suture-anchored tension displayed macroscopic hypertrophy, hardness, erythema, and pruritis up to 3 months. Histologically, scars induced by suture-anchored tension were hypercellular, hypervascular, hyperproliferative with disorganized extracellular matrix deposition, and displayed molecular hallmarks of hypertrophic fibrosis. MiRNA sequencing revealed the different signature in suture-anchored tension induced hypertrophic scars compared to control normal scars.

ORGANISM(S): Mus musculus

PROVIDER: GSE243948 | GEO | 2023/09/28

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Suture-anchored cutaneous tension induces persistent hypertrophic scarring in a novel murine model [RNA-Seq]

Project description:Hypertrophic scars arise from dysregulated wound healing under prolonged mechanical tension, causing disfiguring fibrosis. However, limited preclinical models replicate key features of human tension-induced scarring. We developed an innovative murine model utilizing suture anchoring to impose persistent transverse-axial stretch across healing incisions, mimicking excessive wound tension that leads to hypertrophy clinically. Dorsal paired incisions were generated in mice, with wound edges on the upper back sutured to the rib cage while leaving wound edges on the lower back relaxed. This localized anchoring restrained wound contraction, maintaining high tension throughout remodeling analogous to scars widening under stress. Stretched upper wounds developed profound fibrotic changes compared to relaxed controls. Scars induced by suture-anchored tension displayed macroscopic hypertrophy, hardness, erythema, and pruritis up to 3 months. Histologically, scars induced by suture-anchored tension were hypercellular, hypervascular, hyperproliferative with disorganized extracellular matrix deposition, and displayed molecular hallmarks of hypertrophic fibrosis. MRNA sequencing revealed the fibrogenic signature in suture-anchored tension induced hypertrophic scars, which exhibited transcriptional overlap with mechanically-stretched scars, human hypertrophic and keloid scars.

2023-09-28 | GSE243949 | GEO

Gene expression of hypertrophic scar fibroblasts treated with glucocorticoids under mechanical stretch environment

Project description:After disruption of the skin, fibroblasts along wound edges are constantly exposed to high levels of stress, resulting in increased collagen synthesis and decreased apoptosis. Emerge evidences shows that, the hypertrophic scars tissue fibrosis phenomena are original from the intrinsic cellular mechanical stretch. Traditional glucocorticoids on hypertrophic scarring have been performed for 30 years, utilizing for their anti-inflammatory, anti-allergenic and immunomodulatory effects and for their well-established, pro-apoptotic effects on hematological malignancies. To explore effects of glucocorticoid triamcinolone acetonide for responses to mechanical stress in hypertrophic scars fibroblasts (HSFB), we performed microarrays to explore the differential gene expression.

2020-05-28 | GSE151240 | GEO

Long noncoding RNA (lncRNA) expression profiles of hypertrophic scar fibroblasts treated with glucocorticoids under mechanical stretch environment

Project description:After disruption of the skin, fibroblasts along wound edges are constantly exposed to high levels of stress, resulting in increased collagen synthesis and decreased apoptosis. Emerge evidences shows that, the hypertrophic scars tissue fibrosis phenomena are original from the intrinsic cellular mechanical stretch. Traditional glucocorticoids on hypertrophic scarring have been performed for 30 years, utilizing for their anti-inflammatory, anti-allergenic and immunomodulatory effects and for their well-established, pro-apoptotic effects on hematological malignancies. To explore effects of glucocorticoid triamcinolone acetonide (TA) for responses to mechanical stress in hypertrophic scars fibroblasts (HSFB), we performed microarrays to explore long noncoding RNA expression.

2020-05-26 | GSE151153 | GEO

The Role of the Mammalian Target of Rapamycin in Keloid and Hypertrophic Scars

Project description:We hypothesize that, the mTOR pathway is a dominant pathway in cultured keloid and hypertrophy scar fibriblasts compared to normal skin cells. Certain pathway changes can be detected after medication treatment. Global gene expression in RNA samples from rapamycin and tacrolimus treated fibroblasts (from normal skin and hypertrophic scars, keloid scars) is assayed to study the possibility to use mTOR inhibitors as potential drug to treat abnormal scarring. We investigated the difference between normal wound healing and hypertrophic scars and keloids as well.

2014-05-20 | E-MTAB-2509 | biostudies-arrayexpress

Suture-anchored cutaneous tension induces persistent hypertrophic scarring in a novel murine model

Project description:Suture-anchored cutaneous tension induces persistent hypertrophic scarring in a novel murine model

| PRJNA1020782 | ENA

Suture-anchored cutaneous tension induces persistent hypertrophic scarring in a novel murine model [miRNA]

Project description:Suture-anchored cutaneous tension induces persistent hypertrophic scarring in a novel murine model [miRNA]

| PRJNA1020784 | ENA

Suture-anchored cutaneous tension induces persistent hypertrophic scarring in a novel murine model [RNA-Seq]

Project description:Suture-anchored cutaneous tension induces persistent hypertrophic scarring in a novel murine model [RNA-Seq]

| PRJNA1020785 | ENA

Expression data from the dermis of human stretched scars and patient-matched healthy dermis from occipital scalps

Project description:It is well accepted that elevated mechanical tension of the skin surrounding a healing wound stimulates a fibrotic cascade of events and contributes to an increased size of scars. A laxity paradox in the field of hair transplantation describes a phenomenon opposing this view. During Strip Follicular Unit Transplantation (Strip FUT), surgeons remove a strip of scalp skin (approximately 5 cm x 10 cm, depending on the number of hair follicles required) from the occipital scalp, which is then used to harvest hair follicles that will be transplanted into the balding frontal scalp. Most patients with normal scalp skin laxity heal with narrow normotrophic scars, while a small number of patients (14%) with very loose scalp skin, and so low residual skin tension, heal with post operating scar widening (4 - 12 mm). These scars, referred to as stretched scars in the hair transplantation field, often require revision surgery or secondary hair grafting into the scar. We hypothesise that stretched scars present a unique transcriptional signature different from other types of scars. To determine the gene expression profile of stretched scars, we used Affymetrix microarrays to perform profiling of fibrotic dermis and the surrounding patient-matched healthy dermis.

2022-12-31 | GSE162904 | GEO

High-salt diet promotes hypertrophic scarring through TRPC3-mediated mitochondrial Ca2+ homeostasis dysfunction

Project description:Diet High in salt content have been associated with cardiovascular disease and chronic inflammation. We recently demonstrated that transient receptor potential canonical 3 (TRPC3) channels regulate myofibroblast transdifferentiation in hypertrophic scars. Here, we examined how high salt activation of TRPC3 participates in hypertrophic scarring during wound healing. In vitro, we confirmed that high salt increased the TRPC3 protein expression and the marker of myofibroblast alpha smooth muscle actin (α-SMA) in wild-type mice (WT) primary cultured dermal fibroblasts but not Trpc3-/- mice. Activation of TRPC3 by high salt elevated cytosolic Ca2+ influx and mitochondrial Ca2+ uptake in dermal fibroblasts in a TRPC3-dependent manner. High salt activation of TRPC3 enhanced mitochondrial respiratory dysfunction and excessive reactive oxygen species (ROS) production by inhibiting pyruvate dehydrogenase action, that activated ROS-triggered Ca2+ influx and the Rho kinase/MLC pathway in WT mice but not Trpc3-/- mice. In vivo, a persistent high-salt diet promoted myofibroblast transdifferentiation and collagen deposition in a TRPC3-dependent manner. Therefore, this study demonstrates that high salt enhances myofibroblast transdifferentiation and promotes hypertrophic scar formation through enhanced mitochondrial Ca2+ homeostasis, which activates the ROS-mediated pMLC/pMYPT1 pathway. TRPC3 deficiency antagonizes high salt diet-induced hypertrophic scarring. TRPC3 may be a novel target for hypertrophic scarring during wound healing.

2023-10-24 | PXD042087 | Pride

Single-cell analysis reveals transcriptomic difference between human hypertrophic scar and keloid

Project description:Background Hypertrophic scars and keloids are both pathological scars with similar appearance and pathological features. Currently, the differential diagnosis of the two mainly depends on the subjective judgment of physicians, and there is a lack of objective diagnostic indicators and treatment methods. Objectives To provide single-cell level evidence and new approaches for the differential diagnosis and clinical treatment of hypertrophic scars and keloids. Methods Single-cell RNA sequencing (scRNA-seq) was performed on a hypertrophic scar and a keloid tissue from the same patient to compare the differences in the cellular and tissue microenvironments of the two conditions. Results ScRNA-seq results depicted the distribution of cell subpopulations and different microenvironments between hypertrophic scars and keloids. Conclusions The results of the analysis showed significant differences in cell subcluster distribution and cell communication between hypertrophic scars and keloids. This study demonstrated the potential of scRNA-seq to differentiate the two conditions and provide a new approach to refine differential diagnosis and a possible target for therapeutic research.

2024-11-15 | GSE243716 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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