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Cellular Motility of Down Syndrome Gingival Fibroblasts Is Susceptible to Impairment by Porphyromonas gingivalis Invasion
Author(s) -
Murakami Jumpei,
Kato Takahiro,
Kawai Shinji,
Akiyama Shigehisa,
Amano Atsuo,
Morisaki Ichijiro
Publication year - 2008
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.2008.070400
Subject(s) - porphyromonas gingivalis , periodontal pathogen , motility , integrin , periodontitis , wound healing , paxillin , biology , chemistry , microbiology and biotechnology , immunology , focal adhesion , receptor , signal transduction , medicine , biochemistry
Background: Severe periodontal breakdown is often associated with Down syndrome (DS); however, the etiology of this condition is not understood fully. Cellular motility of gingival fibroblasts is a critical event for wound healing and regeneration of periodontal tissues. Porphyromonas gingivalis is known to be a periodontal pathogen that invades host cells, contributing to periodontal destruction. In this study, we examined the influence of P. gingivalis infection on the motility of DS gingival fibroblasts (DGFs). Methods: DGFs and normal gingival fibroblasts (NGFs) were infected with P. gingivalis with type II fimbriae, and cellular motility was evaluated using an in vitro wounding assay. Protein degradation of α5β1‐integrin subunits and a migration‐regulating signaling molecule, paxillin, were investigated using specific antibodies. The adhesion to and invasion of fibroblasts by P. gingivalis were determined with a colony forming assay. The gene expressions of α5β1‐integrin subunits were also quantified using a reverse transcription‐polymerase chain reaction method. Results: The cellular motility of DGFs was impaired significantly by P. gingivalis compared to NGFs, and the former were invaded readily by P. gingivalis . Further, cellular paxillin from DGFs was degraded markedly by the pathogen. Although protein degradation of α5β1 integrin was induced, its mRNA expression was not affected significantly. Conclusions: P. gingivalis readily invades DGFs and subsequently degrades paxillin, which impairs cellular motility and likely prevents wound healing and the regeneration of periodontal tissues. These characteristics may be involved in the etiology of DS periodontitis.