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• W2092314446 abstract "In vivo, fibroblasts reside in connective tissues, with which they communicate in a reciprocal way. Such cell--extracellular matrix interactions can be studied in vitro by seeding fibroblasts in collagen lattices. Depending upon the mechanical properties of the system, fibroblasts are activated to assume defined phenotypes. In the present study, we examined a transcriptional profile of primary human dermal fibroblasts cultured in a relaxed collagen environment and found relative induction (>2-fold) of 393 out of approx. 7100 transcripts when compared with the same system under mechanical tension. Despite down-regulated proliferation and matrix synthesis, cells did not become generally quiescent, since they induced transcription of numerous other genes including matrix metalloproteinases (MMPs) and growth factors/cytokines. Of particular interest was the induction of gene transcripts encoding pro-inflammatory mediators, e.g. cyclo-oxygenase-2 (COX-2), and interleukins (ILs)-1 and -6. These are apparently regulated in a hierarchical fashion, since the addition of IL-1 receptor antagonist prevented induction of COX-2, IL-1 and IL-6, but not that of MMP-1 or keratinocyte growth factor (KGF). Our results suggest strongly that skin fibroblasts are versatile cells, which adapt to their extracellular environment by displaying specific phenotypes. One such phenotype, induced by a mechanically relaxed collagen environment, is the 'pro-inflammatory' fibroblast. We propose that fibroblasts that are embedded in a matrix environment can actively participate in the regulation of inflammatory processes." @default.
• W2092314446 created "2016-06-24" @default.
• W2092314446 creator A5008944785 @default.
• W2092314446 creator A5070111191 @default.
• W2092314446 creator A5078749744 @default.
• W2092314446 date "2004-04-15" @default.
• W2092314446 modified "2023-09-23" @default.
• W2092314446 title "Expression of pro-inflammatory markers by human dermal fibroblasts in a three-dimensional culture model is mediated by an autocrine interleukin-1 loop" @default.
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• W2092314446 doi "https://doi.org/10.1042/bj20031371" @default.
• W2092314446 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1224070" @default.
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• W2092314446 hasPublicationYear "2004" @default.
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