Dyspigmented hypertrophic scars: Beyond skin color
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA664128 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Although pigment synthesis is well understood, relevant mechanisms of psychologically debilitating dyspigmentation in nascent tissue after cutaneous injuries are still unknown. Here, differences in genomic transcription of hyper- and hypopigmented tissue relative to uninjured skin were investigated using a red Duroc swine scar model. Transcription profiles differed based on pigmentation phenotypes with a trend of more upregulation or downregulation in hyper- or hypopigmented scars, respectively. Ingenuity Pathway Analysis of significantly modulated genes in both pigmentation phenotypes showed pathways related to redox, metabolic, and inflammatory responses were more present in hypopigmented samples, while those related to stem cell development differentiation were found mainly in hyperpigmented samples. Cell-cell and cell-extracellular matrix interactions and inflammation responses were predicted (z-score) active in hyperpigmented and inactive in hypopigmented. The proinflammatory high-mobility group box 1 pathway showed the opposite trend. Analysis of differentially regulated mutually exclusive genes showed an extensive presence of metabolic, proinflammatory, and oxidative stress pathways in hypopigmented scars, while melanin synthesis, glycosaminoglycans biosynthesis, and cell differentiation pathways were predominant in hyperpigmented scar. Several potential therapeutic gene targets have been identified.
2020-09-17 | GSE158155 | GEO
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
Project description: Not available
| S-EPMC6697599 | biostudies-literature
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
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
Project description:Hypertrophic skin scarring following dermal injury causes extreme pain and psychological trauma for patients. Unfortuately, we do not have effective treatments to prevent or reverse skin scarring. Using RNA and ATAC sequencing of mouse and human fibroblasts, we show that JUN expressing fibroblasts are responsible for skin scarring by regulating CD36 expression. In summary, we show that CD36 antagonism by represent a therapeutic target to overcome JUN hypertrophic skin scarring.
2021-06-22 | GSE178562 | GEO
Project description:Hypertrophic scarring (HS) is characterized by excessive extracellular matrix deposition, matrix metalloprotein gene activation, and fibroblast invasive growth. However, the methylation level of hypertrophic scarring is poorly understood. Genome wide DNA methylation profiling of normal skin and hypertrophic scar. The Illumina Infinium Methylation EPIC BeadChip (850K) was used to obtain DNA methylation profiles across approximately 853,307 CpGs in liquid based scar samples. Samples included 6 normal skin, and 6 hypertrophic scar.
2023-04-20 | GSE229848 | GEO
Project description:Pentoxifylline attenuated hypertrophic scars by influencing the cell cycles
2019-07-09 | GSE122891 | GEO
Project description:Keloids are scars that extend beyond original wounds and are resistant to treatment. In order to improve understanding of the molecular basis of keloid scarring, we have assessed the genomic profiles of keloid fibroblasts and keratinocytes. Skin and scar tissues were obtained for isolation of primary keratinocytes and fibroblasts. Keloid scars were excised from patients undergoing scar excision surgery, normal skin samples were isolated from patients undergoing elective plastic surgery. Primary culters were prepared for keratinocytes and fibroblasts, and were harvested for analysis up to passage three. Nine keloid scars, for adjacent non-lesional keloid skin samples, and three normal skin samples were obtained and cultured. RNA was isolated using RNeasy, and quality verified using an Agilent 2100 Bioanalyzer. Labeling and hybridization to Affymetrix Human Gene 1.0 ST microarray chips was performed by the Vanderbilt Genome Sciences Resource at Vanderbilt University Medical Center.
2013-05-28 | E-GEOD-44270 | biostudies-arrayexpress
Project description:Keloid scars is a pathologic fibro-proliferative disorders of the skin, which exhibit abnormal phenotypes including fibroblasts proliferation and collagen deposits. There have been several treatments of keloids including conventional surgical therapies and adjuvant therapies, but a high recurrence rate of keloids was also observed after treatment. Quantitative proteomics approach has been proved an efficient approach to investigate pathological mechanism and novel biomarkers. In this study, we present a label-free quantitative proteomics analysis to explore differential protein expression profiles in normal skin and keloid scar tissues based on nano-liquid chromatography and tandem mass spectrometry (Nano-LC–MS/MS). The study results displayed a more comprehensive keloid protein expression landscape and provided novel pathological insight of keloid.
2023-03-11 | PXD029631 | Pride