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14 Ergebnisse
The role of stem cell factor and c-KIT in keloid pathogenesis: do tyrosine kinase inhibitors have a potential therapeutic role?
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BACKGROUND
Keloids are fibroproliferative disorders characterized by increased deposition of extracellular matrix components. Stem cell factor (SCF) and its receptor c-KIT are expressed in a wide variety of cells and have also been demonstrated to be important modulators of the wound healing
Cellular signaling by tyrosine phosphorylation in keloid and normal human dermal fibroblasts.
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Keloids represent a dysregulated response to cutaneous wounding that results in disfiguring scars. Unique to humans, keloids are characterized by an accumulation of extracellular matrix components. The underlying molecular mechanisms of keloid pathogenesis, however, remain largely uncharacterized.
Identification and characterization of Wnt signaling pathway in keloid pathogenesis.
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Keloid is characterized by fibroblastic cell proliferation and abundant collagen synthesis. Numerous studies have shown that the Wingless type (Wnt) signaling pathways play key roles in various cellular functions including proliferation, differentiation, survival, apoptosis and migration. The aim of
Pleiotrophin is downregulated in human keloids.
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Keloid is an abnormal hyperproliferative scarring process with involvement of complex genetic and triggering environmental factors. Previously published dysregulated gene expression profile of keloids includes genes involved in tumor formation. Pleiotrophin (PTN) is a secreted, heparin-binding
Phosphorylation of extracellular signal-regulated protein kinase in cultured keloid fibroblasts when stimulated by platelet-derived growth factor BB.
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Abnormal scars result in distressing symptoms and disfiguring blemishes; an understanding of the molecular events that cause such scars, particularly keloids, would make possible the optimisation of both wound healing and treatment. Extracellular signal-regulated protein kinase (ERK) has a crucial
The effect of suppressing discoidin domain receptor expression on keloid formation and proliferation .
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BACKGROUND
Discoidin domain receptors (DDR) with tyrosine kinase activity have been identified as novel receptors for modulating collagen production and organization in scar tissue. The purpose of this study was to explore the effect of blocking discoidin domain receptor 1 (DDR1), signaling of
Crosstalk of hypoxia-mediated signaling pathways in upregulating plasminogen activator inhibitor-1 expression in keloid fibroblasts.
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Keloids are skin fibrotic conditions characterized by an excess accumulation of extracellular matrix (ECM) components secondary to trauma or surgical injuries. Previous studies have shown that plasminogen activator inhibitor-1 (PAI-1) can be upregulated by hypoxia and may contribute to keloid
Overexpression of insulin-like growth factor-1 (IGF-I) receptor and the invasiveness of cultured keloid fibroblasts.
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Keloid is a dermal fibroproliferative tissue of unknown etiology. Protein tyrosine kinases (PTKs) play an important role in the regulation of cell growth and differentiation. Activation of PTK cascades in keloid fibroblasts is thought to be closely linked to abnormal cell proliferation and
Nintedanib inhibits keloid fibroblast functions by blocking the phosphorylation of multiple kinases and enhancing receptor internalization.
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Keloid is a benign skin tumor characterized by its cell hyperproliferative activity, invasion into normal skin, uncontrolled growth, overproduction and deposition of extracellular matrices and high recurrence rate after various therapies. Nintedanib is a receptor tyrosine kinase inhibitor targeting
Recurrent, Activating Variants in the Receptor Tyrosine Kinase DDR2 Cause Warburg-Cinotti Syndrome.
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We have investigated a distinct disorder with progressive corneal neovascularization, keloid formation, chronic skin ulcers, wasting of subcutaneous tissue, flexion contractures of the fingers, and acro-osteolysis. In six affected individuals from four families, we found one of two recurrent
A Role for Neuregulin-1 in Promoting Keloid Fibroblast Migration via ErbB2-mediated Signaling.
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Keloid disease is a fibroproliferative tumour characterised by aggressive local invasion, evident from a clinically and histologically active migrating margin. During combined laser capture microdissection and microarray analysis-based in situ gene expression profiling, we identified upregulation of
Sodium L-ascorbate enhances elastic fibers deposition by fibroblasts from normal and pathologic human skin.
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BACKGROUND
Vitamin C (L-ascorbic acid), a known enhancer of collagen deposition, has also been identified as an inhibitor of elastogenesis.
OBJECTIVE
Present studies explored whether and how the L-ascorbic acid derivative (+) sodium L-ascorbate (SA) would affect production of collagen and elastic
Etk/Bmx mediates expression of stress-induced adaptive genes VEGF, PAI-1, and iNOS via multiple signaling cascades in different cell systems.
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We recently showed that Etk/Bmx, a member of the Tec family of nonreceptor protein tyrosine kinases, promotes tight junction formation during chronic hypoxic exposure and augments normoxic VEGF expression via a feedforward mechanism. Here we further characterized Etk's role in potentiating
Silk-fibroin-coated liposomes for long-term and targeted drug delivery.
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Many barriers to drug delivery into a tumor site require careful consideration when designing a new drug. In this study, the adhesive targeting and drug specificity of modified liposomal vesicles on human-scar-producing cells, keloid fibroblasts, were investigated. Keloids express abundant levels of
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