Abstract
Background:
Keloids are benign proliferations of fibroblasts, but their exact etiology and molecular pathogenesis are unknown.
Materials and methods:
Fibroblasts were isolated from the central and peripheral regions of keloids, and the growth behavior and molecular characteristics of the keloid fibroblasts were compared with those of age-adjusted normal dermal fibroblasts.
Results:
Central (but not peripheral) keloid fibroblasts exhibited significantly increased growth and high levels of expression of transforming growth factor-beta (TGF-beta) receptor 1 and Smad 2/3.
Conclusion:
Proliferation of central keloid fibroblasts, which results in keloid formation, appears to mainly involve the TGF-beta/Smad pathway.
MeSH terms
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Actins / metabolism
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Activin Receptors, Type I / metabolism
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Adolescent
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Adult
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Blotting, Western
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Cell Culture Techniques
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Cell Proliferation
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Cell Survival
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Cells, Cultured
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Female
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Fibroblasts / metabolism
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Fibroblasts / physiology*
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Humans
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Keloid / metabolism
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Keloid / physiopathology*
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Kinetics
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Male
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Middle Aged
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Protein Serine-Threonine Kinases
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Receptor, Transforming Growth Factor-beta Type I
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Receptor, Transforming Growth Factor-beta Type II
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Receptors, Transforming Growth Factor beta / metabolism
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Signal Transduction*
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Skin / cytology
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Smad Proteins / metabolism*
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Smad2 Protein / metabolism
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Smad3 Protein / metabolism
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Smad4 Protein / metabolism
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Transforming Growth Factor beta / metabolism*
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Up-Regulation
Substances
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Actins
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Receptors, Transforming Growth Factor beta
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SMAD2 protein, human
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SMAD3 protein, human
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SMAD4 protein, human
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Smad Proteins
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Smad2 Protein
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Smad3 Protein
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Smad4 Protein
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Transforming Growth Factor beta
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Protein Serine-Threonine Kinases
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Activin Receptors, Type I
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Receptor, Transforming Growth Factor-beta Type I
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Receptor, Transforming Growth Factor-beta Type II