نتایج جستجو برای: dermal fibroblasts
تعداد نتایج: 75227 فیلتر نتایج به سال:
BACKGROUND Keloid and hypertrophic scar (HS) are two pathological forms of excessive dermal fibrosis, which are due to aberrant wound-healing responses. Accumulating evidence suggests that aberrant activity of growth factors and increased numbers of growth factor receptors play an important role in the formation of pathological scar. AIM We examined the expression level of insulin-like growth...
This study aimed to understand the role of the matrix polysaccharide, hyaluronan (HA), in influencing the scarring process by assessing its impact on regulating fibroblast behavior. Donor-matched human oral and dermal fibroblasts were used as models of nonscarring and scarring fibroblast phenotypes, respectively. Phenotypic differences in these two fibroblast populations were assessed and relat...
UNLABELLED 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 keloid fibroblast cells on the inhibition of keloid formation, and proliferation, by m...
Keloids, partially considered as benign tumors, are characterized by the overgrowth of fibrosis beyond the boundaries of the wound and are regulated mainly by transforming growth factor (TGF)-β1, which induces the transition of fibroblasts to myofibroblasts. Hypoxia is an important driving force in the development of lung and liver fibrosis by activating hypoxia inducible factor-1α and stimulat...
A common feature of some parasitic infections and allergic and atopic skin diseases is the involvement of Th2 lymphocytes and the dermal appearance of eosinophils (Eos). Because Th2 lymphocytes apparently do not release Eo attractants, we addressed the question of whether the Th2 cytokine IL-4 induces its production in dermal fibroblasts. We therefore stimulated fibroblasts with IL-4. HPLC inve...
Decreased or impaired proliferation capability of dermal fibroblasts interferes with successful wound healing. Several growth factors tested failed to fully restore the growth of fibroblasts, possibly due to their rapid degradation by proteases. It is therefore critical to find new agents which have stimulatory effects on fibroblasts while being highly resistant to degradation. In such a scenar...
Mast cell tryptase stimulates human lung fibroblast proliferation via protease-activated receptor-2.
Mast cells play a potentially important role in fibroproliferative diseases, releasing mediators including tryptase that are capable of stimulating fibroblast proliferation and procollagen synthesis. The mechanism by which tryptase stimulates fibroblast proliferation is unclear, although recent studies suggest it can activate protease-activated receptor (PAR)-2. We therefore investigated the ro...
Fibroblasts and their activated phenotype, myofibroblasts, are the primary cell types involved in the contraction associated with dermal wound healing. Recent experimental evidence indicates that the transformation from fibroblasts to myofibroblasts involves two distinct processes: The cells are stimulated to change phenotype by the combined actions of transforming growth factor β (TGFβ) and me...
OBJECTIVE To assess dermal expression and fibroblast production of fibrillin-1 (FBN-1) in SSc. METHODS In vivo analysis of microfibrillar network was performed using EM from affected and unaffected skin biopsy specimens of dcSSc patients (n = 5) compared with healthy controls (n = 2). FBN-1 matrix deposition and organization by dermal fibroblast cultures from dcSSc (n = 6), healthy (n = 5) an...
The dermis is largely composed of collagen-rich fibrils that form a dense extracellular matrix (ECM). Dermal fibroblasts produce and are embedded within the dermal ECM. During aging, ECM becomes fragmented. This fragmentation associated with deleterious alterations fibroblast function. We have investigated degree to which these stem from adaptation deterioration versus cell-autonomous age-drive...
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