The TGF-beta 1-mediated increase in keloid fibronectin production is independent of the steroid regulatory pathway for fibronectin, which accelerates synthesis by means of a post-transcriptional mechanism.
The TGF-beta 1-mediated increase in keloidfibronectin production is independent of the steroid regulatory pathway for fibronectin, which accelerates synthesis by means of a post-transcriptional mechanism.
Although stimulation of transcription may not entirely account for the increase in fibronectin biosynthesis in keloids, this mechanism is best able to account for the majority of the change.
These data indicate that the rate of gene transcription of alpha 1(I) procollagen is increased in both hypertrophic scars and keloids, but only keloids exhibit increased steady-state levels of alpha 1(I) procollagen mRNA and concurrent increases in type I collagen.
In this study, we investigated the potential of bFGF to regulate the expression of various dermal extracellular matrix proteoglycans and type I collagen mRNAs in cultured human fibroblasts from keloid, which is a prototype of dermal fibrosis, and normal skin tissue.
One group of cells (NSk, NSc and keloid) were exposed to 10 ng/mL of exogenous TGF-beta1 for 24 hours, while the other group was used as control with no exposure to exogenous TGF-beta1.
Collectively, these data suggest that (1) specific controls on PAI-1 gene expression are fundamentally different between these two clinically significant high PAI-1-synthesizing cell types and (2) the localized keloid may define the emergence of a distinct profibrotic dermal fibroblastoid phenotype in genetically predisposed individuals.
Differential effects of hexoses and sucrose, and platelet-derived growth factor isoforms on cyclooxygenase-1 and -2 mRNA expression in keloid, hypertrophic scar and granulation tissue fibroblasts.
In contrast, the remarkably elevated MMP-13 mRNA expression in the keloid group was significantly suppressed, with the peak suppression at 12 h after addition of tretinoin, while MMP-13 mRNA expression in the control group was not significantly changed.
These results indicate that insulin-like growth factor-I enhances transforming growth factor-beta-inducedkeloid formation through transforming growth factor-beta postreceptor signal cross-talk, mainly via the p38 mitogen-activated protein kinase/activating transcription factor-2 pathway.
Comparison of transforming growth factor-beta/Smad signaling between normal dermal fibroblasts and fibroblasts derived from central and peripheral areas of keloid lesions.