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Hypoxia-induced HIF-1 alpha accumulation is augmented in a co-culture of keloid fibroblasts and human mast cells: involvement of ERK1/2 and PI-3K/Akt.
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Keloids represent a prolonged inflammatory fibrotic state with areas that display distinctive histological features characterized by an abundant extracellular matrix stroma, a local infiltration of inflammatory cells including mast cells, and a milieu of enriched cytokines. Previous studies from our
[Different effects of simvastatin on keloid fibroblasts under hypoxia and TGF-β1 treatment].
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To explore the effect of simvastatin on the proliferation, apoptosis and protein expressions of keloid fibroblasts under normoxia,hypoxia or TGF-β1 treatment.
Keloid fibroblasts (KFs) were isolated by explants culture method. KFs were treated with different concentrations of simvastatin under
[The effects of conditioned medium from keloid fibroblasts under hypoxia on angiogenesis].
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OBJECTIVE
To observe the effects of conditioned medium from keloid fibroblasts under hypoxia on angiogenesis, and to investigate the role of hypoxic microenvironment in invasive growth of keloid.
METHODS
Primary keloid fibroblasts and human umbilical endothelial cells (HUVEC) were cultured as
Hypoxia upregulates VEGF production in keloid fibroblasts.
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The etiology of keloid formation is diverse. They are characterized grossly as thick scar tissue that extends beyond the boundaries of the original wound. Histologically, keloids are composed of excessive collagen with an abnormally large number of partially or totally occluded microvessels. This
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
Role of Hypoxia Inducible Factor-1 Alpha (HIF-1α) in Cytoglobin Expression and Fibroblast Proliferation of Keloids.
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Hypoxia and HIF-1α Regulate Collagen Production in Keloids.
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Keloids are reactive or spontaneous fibroproliferative dermal tumors characterized by the exaggerated and uncontrolled accumulation of extracellular collagen. Current approaches to mitigate keloidogenesis are largely procedural in nature. However, a better understanding of its biological drivers may
Elevated vascular endothelial growth factor in keloids: relevance to tissue fibrosis.
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Excessive scar or keloid shares common features of a benign dermal growth. Yet, in contrast to malignant tumor, a keloid does not expand beyond the dermis. What triggers the continuing growth of a benign lesion? Deficient or overabundant levels of vascular endothelial growth factor have been
Central regions of keloids are severely ischaemic.
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We classified scars as keloids, hypertrophic scars and mature scars, and then examined the scars for differences in central and marginal vascularization. We found significant differences in localized hypoxia-induced factor-1α (HIF-1α) expression and vascular density in keloids, but no localized
Sumoylation enhances the activity of the TGF-β/SMAD and HIF-1 signaling pathways in keloids
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Excessive fibrosis and extracellular matrix deposition resulting from upregulation of target genes expression mediated by transforming growth factor-beta (TGF-β)/SMAD and hypoxia inducible factor-1 (HIF-1) signaling pathways are the main mechanisms that drive keloid formation. Sumoylation is a
Expressions of Collagen I and III in Hypoxic Keloid Tissue.
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BACKGROUND
Wound heals itself spontaneously as physiological process. However, in some individuals, small wounds such as parenteral injections or body piercings may cause increased expression of collagen synthesis. The condition is known as keloid. Histopathology of keloid demonstrates extensive
Hyperbaric oxygen therapy can ameliorate the EMT phenomenon in keloid tissue.
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BACKGROUND
Hyperbaric oxygen therapy (HBOT) has been widely used in the clinical setting. In this study, HBOT therapy was evaluated for its ability to ameliorate the epithelial-to-mesenchymal transition (EMT) phenomenon in keloid tissue.
METHODS
Keloid patients were randomly divided into two groups:
The histotopographic features of formation of keloid scars of maxillofacial localization.
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The microvessels in hypertrophic scars, keloids and related lesions: a review.
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The healing of a deep surface wound in humans begins with the formation of granulation tissue and includes a marked microvascular regeneration, initially in an inflammatory milieu. The inevitable sequel is usually a hypertrophic scar or keloid in which there is significant microvascular occlusion.
Mechanisms of hypoxic regulation of plasminogen activator inhibitor-1 gene expression in keloid fibroblasts.
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Keloids are an excessive accumulation of extracellular matrix. Although numerous studies have shown elevated plasminogen activator inhibitor-1 (PAI-1) levels in keloid fibroblasts compared with those of normal skin. Their specific mechanisms involved in the differential expression of PAI-1 in these
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