Abstract

Keloids result from pathological wound healing responses. However, the pathogenesis of keloids is still poorly understood. PGE 2 was shown to decrease fibroblast proliferation, inhibit collagen synthesis and enhance the expression of matrix-metalloproteinases (MMPs). This study sought to delineate the production of PGE 2 by normal and keloid-derived dermal fibroblasts. Human normal and keloid dermal fibroblasts were cultured in vitro. Cell proliferation and viability were determined based on WST-1 assay. IL-1β-induced PGE 2 production and effects of PGE 2 on the synthesis of procollagen by culture-derived fibroblasts were determined by using enzyme-linked immunosorbant assay (ELISA) kits. IL-1β-induced MMP-1 production by culture-derived fibroblasts was determined with an MMP-1 immunoassay kit. Our results showed that normal and keloid-derived fibroblasts exhibited a statistically significant increase ( p < 0.05) in cell proliferation when the cells were cultured in media with an increase in the concentrations (0%, 2% and 10%) of fetal bovine serum (FBS). In culture medium without FBS, an increase in cell proliferation of keloid-derived fibroblasts was detectable when compared with those of control fibroblasts. IL-1β (1 ng/ml and 10 ng/ml) stimulated statistically significant production ( p < 0.01) of PGE 2 by both normal and keloid-derived fibroblasts. However, lower levels of PGE 2 produced by keloid-derived fibroblasts were detectable compared with those produced by normal-derived fibroblasts ( p < 0.05). In this study, although not statistically significant, inhibition of procollagen production by PGE 2 in a dose-dependent manner was found. In addition, decreased production of MMP-1 by keloid-derived fibroblasts compared with those of control fibroblasts was also observed. In conclusion, keloid-derived fibroblasts produced less PGE 2 than those produced by control fibroblasts. The role of diminished capacity of PGE 2 production in keloid formation is presently unknown and needs further study.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call