Journal
JOURNAL OF PERIODONTOLOGY
Volume 85, Issue 4, Pages 627-635Publisher
AMER ACAD PERIODONTOLOGY
DOI: 10.1902/jop.2013.120703
Keywords
Anti-inflammatory agents; cell biology; cytokines; fibroblasts; guided tissue regeneration, periodontal; wounds and injuries
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Funding
- International Team for Implantology, Basel, Switzerland [RCL 653]
- Austrian Science Fund (FWF) [J3379-B19]
- Austrian Science Fund (FWF) [J 3379] Funding Source: researchfish
- Austrian Science Fund (FWF) [J3379] Funding Source: Austrian Science Fund (FWF)
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Background: The use of prolyl hydroxylase inhibitors such as L-mimosine (L-MIM) and dimethyloxaloylglycine (DMOG) to improve angiogenesis is a new approach for periodontal regeneration. In addition to exhibiting pro-angiogenic effects, prolyl hydroxylase inhibitors can modulate the plasminogen activator system in cells from non-oral tissues. This study assesses the effect of prolyl hydroxylase inhibitors on plasminogen activation by fibroblasts from the periodontium. Methods: Gingival and periodontal ligament fibroblasts were incubated with L-MIM and DMOG. To investigate whether prolyl hydroxylase inhibitors modulate the net plasminogen activation, kinetic assays were performed with and without interleukin (IL)-1. Moreover, plasminogen activators and the respective inhibitors were analyzed by casein zymography, immune assays, and quantitative polymerase chain reaction. Results: The kinetic assay showed that L-MIM and DMOG reduced plasminogen activation under basal and IL-1-stimulated conditions. Casein zymography revealed that the effect of L-MIM involves a decrease in urokinase-type plasminogen activator activity. In agreement with these findings, reduced levels of urokinase-type plasminogen activator and elevated levels of plasminogen activator inhibitor 1 were observed. Conclusion: L-MIM and DMOG can reduce plasminogen activation by fibroblasts from the gingiva and the periodontal ligament under basal conditions and in the presence of an inflammatory cytokine.
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