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Gene expression 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 for responses to mechanical stress in hypertrophic scars fibroblasts (HSFB), we performed microarrays to explore the differential gene expression.

ORGANISM(S): Homo sapiens

PROVIDER: GSE151240 | GEO | 2020/05/28

REPOSITORIES: GEO

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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.

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

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METTL3 Facilitates Hypertrophic Scar Fibrosis by Promoting pri-miRNA-31 Maturation and ZBTB20 Silencing in m6A-dependent Manner [RNA-Seq]

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