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l ‐Mimosine and Dimethyloxaloylglycine Decrease Plasminogen Activation in Periodontal Fibroblasts
Author(s) -
Wehner Christian,
Gruber Reinhard,
Agis Hermann
Publication year - 2014
Publication title -
journal of periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.036
H-Index - 156
eISSN - 1943-3670
pISSN - 0022-3492
DOI - 10.1902/jop.2013.120703
Subject(s) - plasminogen activator , chemistry , zymography , urokinase , microbiology and biotechnology , matrix metalloproteinase , biochemistry , endocrinology , medicine , biology
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.