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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE151153 | GEO | 2020/05/26

REPOSITORIES: GEO

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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

Glucocorticoid promotes fatty acids metabolism in hypertrophic scar tissues and fibroblasts via the microRNA

Project description:Hypertrophic scar (HS) is a skin lesion due to abnormal wound healing after skin injury; histologically, HS is characterized by deposition of excessive amounts of the extracellular matrix and collagen produced by wound healing-induced proliferative fibroblasts. Clinically, HS management includes surgical resection of HS, topical glucocorticoid therapy or drug injections, pressure therapy, fractional carbon dioxide laser therapy, and cryotherapy. In terms of non-surgical therapy, glucocorticoids (like Triamcinolone acetonide, a synthetic corticosteroid medication used topically to treat various skin conditions) was able to effectively inhibit HS formation safely for decades. The effects of glucocorticoids may either be due to its anti-inflammatory, anti-allergenic and immunomodulatory effects or activate fatty acids metabolism by promotion of lipid accumulation in fibroblasts. However, it is no clear why and how glucocorticoids-upregulated fatty acid metabolisms benefit in HS treatment and prevention.And it remains to be defined how altered microRNAs regulated-fatty acid metabolism involved in pathological scars.

2023-02-25 | GSE225646 | GEO

Pentoxifylline-induced differentially-expressed genes in hypertrophic scar fibroblasts

Project description:Pentoxifylline attenuated hypertrophic scars by influencing the cell cycles

2019-07-09 | GSE122891 | GEO

Gene Expression in Three Early Human Hypertrophic Scar Samples

Project description:The goal was to obtain expression data from the deep cones in early human hypertrophic scars to be used to confirm expression data obtained in a porcine model. Three samples of early human hypertrophic scar were obtained and processed with the Affymetrix Human GeneChip® Human Genome U133 plus 2.0. Sample demographics were Black 2, White 1; upper extremity 2, neck 1; times since injury 6.7 months and 10.8 months; and patient ages were 19 and 54.

2011-12-31 | E-GEOD-26213 | biostudies-arrayexpress

Gene Expression in Three Early Human Hypertrophic Scar Samples

Project description:The goal was to obtain expression data from the deep cones in early human hypertrophic scars to be used to confirm expression data obtained in a porcine model.

2011-12-31 | GSE26213 | 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

Keratinocyte and fibroblast gene expression in skin and keloid scar tissue

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

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

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

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. MiRNA sequencing revealed the different signature in suture-anchored tension induced hypertrophic scars compared to control normal scars.

2023-09-28 | GSE243948 | GEO

Effect of glucocorticoid chemical structure and receptor potency on human trabecular meshwork cells

Project description:Glucocorticoids with different chemical structures but similar glucocorticoid receptor potency regulate subsets of common and unique genes in human trabecular meshwork cells. Gene expression changes of human trabecular meshwork cells, TM 86 and TM 93, due to treatment with dexamethasone (Dex), fluocinolone acetonide (FA), and triamcinolone acetonide (TA).

2010-02-15 | GSE16643 | GEO

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