Interleukin-1 regulation of procollagenase mRNA and protein in periodontal fibroblasts in vitro

An in vitro model is used to investigate the hypothesis that activated fibroblasts produce collagenolytic activity in inflammatory sites. Interleukin‐1, a cytokine present in the gingiva and crevicular fluid of periodontitis patients, has multiple biologic activities including the ability to stimula...

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Veröffentlicht in:Journal of periodontal research 1990-07, Vol.25 (4), p.222-229
Hauptverfasser: Richards, David, Rutherford, R. Bruce
Format: Artikel
Sprache:eng
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Zusammenfassung:An in vitro model is used to investigate the hypothesis that activated fibroblasts produce collagenolytic activity in inflammatory sites. Interleukin‐1, a cytokine present in the gingiva and crevicular fluid of periodontitis patients, has multiple biologic activities including the ability to stimulate collagenase in dermal and synovial fibroblasts. In this report IL‐1 is tested on gingival (GF) and periodontal ligament fibroblasts (PLF) for its ability to increase collagenolytic activity and procollagenase mRNA and protein. GF produce a 3‐ to 7‐fold increase in collagenase activity, while PLF collagenase activity is rarely increased above control amounts by IL‐1 treatment. In contrast, both cell types demonstrate an increase in procollagenase protein production with IL‐1 treatment. RNA from both GF and PLF contain procollagenase mRNA as demonstrated when northern blots of fibroblast total RNA are hybridized with the cDNA for human procollagenase. Treatment with IL‐1 increases the steady‐state levels of this message in GF by up to 10‐fold in 48 hours when measured with dot blot analysis standardized for poly‐A RNA. PLF also produce up to 7 times more message at the same dose and time. Since fibroblasts present in the lesion are exposed to inflammatory cell products it is possible that the production of collagenase by these cells could result in the destruction of the periodontal fibrous attachment.
ISSN:0022-3484
1600-0765
DOI:10.1111/j.1600-0765.1990.tb00908.x