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Classification analysis of the transcriptosome of nonlesional cultured dermal fibroblasts from systemic sclerosis patients with early disease.
TLDR
Fibroblasts cultured from nonlesional skin of patients with SSc already have detectable abnormalities in a variety of genes and cellular processes, including those involved in extracellular matrix formation, fibrillogenesis, complement activation, and angiogenesis. Expand
Association of novel polymorphisms with the expression of SPARC in normal fibroblasts and with susceptibility to scleroderma.
TLDR
This study is the first to show that polymorphisms of the SPARC gene are associated with susceptibility to, and clinical manifestations of, SSc and that they may also be functionally important in influencing SPARC expression in skin fibroblasts. Expand
Abnormalities in fibrillin 1-containing microfibrils in dermal fibroblast cultures from patients with systemic sclerosis (scleroderma).
TLDR
Although SSc fibroblasts assemble microfibrils, these microfafibrils are unstable, suggesting that an inherent defect of fibrillin 1-containing microFibrils may play a role in the pathogenesis of SSc. Expand
Profibrillin‐1 maturation by human dermal fibroblasts: Proteolytic processing and molecular chaperones
TLDR
This report provides evidence that profibrillin‐1 processing is not an intracellular event, and delineate the secretion and proteolytic processing of profibrisin‐1, and identify the proteins that interact with Profibrillin-1 in the secretory pathway. Expand
Small interfering RNA inhibition of SPARC attenuates the profibrotic effect of transforming growth factor β1 in cultured normal human fibroblasts
TLDR
Specific inhibition of SPARC led to decreased expression of type I collagen and attenuated the profibrotic effect of TGFβ1 in cultured normal human fibroblasts, indicating a potential therapeutic approach to fibrotic disorders such as scleroderma. Expand
Small interfering RNA inhibition of SPARC attenuates the profibrotic effect of transforming growth factor beta1 in cultured normal human fibroblasts.
TLDR
Specific inhibition of SPARC led to decreased expression of type I collagen and attenuated the profibrotic effect of TGFbeta1 in cultured normal human fibroblasts, which represents a potential therapeutic approach to fibrotic disorders such as scleroderma. Expand