|Title:||Butyrate induces reactive oxygen species production and affects cell cycle progression in human gingival fibroblasts||Authors:||Chang M.-C.
|Issue Date:||2013||Journal Volume:||48||Journal Issue:||1||Start page/Pages:||1058-1062||Source:||Journal of Periodontal Research||Abstract:||
Background and Objective: Short-chain fatty acids, such as butyric acid and propionic acid, are metabolic by-products generated by periodontal microflora such as Porphyromonas gingivalis, and contribute to the pathogenesis of periodontitis. However, the effects of butyrate on the biological activities of gingival fibroblasts (GFs) are not well elucidated. Material and Methods: Human GFs were exposed to various concentrations of butyrate (0.5-16mm) for 24h. Viable cells that excluded trypan blue were counted. Cell cycle distribution of GFs was analyzed by propidium iodide-staining flow cytometry. Cellular reactive oxygen species (ROS) production was measured by flow cytometry using 2',7'-dichlorofluorescein (DCF). Total RNA and protein lysates were isolated and subjected to RT-PCR using specific primers or to western blotting using specific antibodies, respectively. Results: Butyrate inhibited the growth of GFs, as indicated by a decrease in the number of viable cells. This event was associated with an induction of G0/G1 and G2/M cell cycle arrest by butyrate (4-16mm) in GFs. However, no marked apoptosis of GFs was noted in this experimental condition. Butyrate (>2mm) inhibited the expression of cdc2, cdc25C and cyclinB1 mRNAs and reduced the levels of Cdc2, Cdc25C and cyclinB1 proteins in GFs, as determined using RT-PCR and western blotting, respectively. This toxic effect of butyrate was associated with the production of ROS. Conclusion: These results suggest that butyrate generated by periodontal pathogens may be involved in the pathogenesis of periodontal diseases via the induction of ROS production and the impairment of cell growth, cell cycle progression and expression of cell cycle-related genes in GFs. These events are important in the initiation and prolongation of inflammatory processes in periodontal diseases. ? 2012 John Wiley & Sons A/S.
|ISSN:||0022-3484||DOI:||10.1111/j.1600-0765.2012.01504.x||metadata.dc.subject.other:||2',7'-dichlorofluorescein; butyric acid derivative; CCNB1 protein, human; CDC2 protein, human; CDC25C protein, human; coloring agent; cyclin B; cyclin B1; diagnostic agent; dichlorofluorescein; fluorescein derivative; fluorescein isothiocyanate; fluorescent dye; propidium iodide; protein tyrosine phosphatase; reactive oxygen metabolite; apoptosis; article; cell cycle; cell cycle G0 phase; cell proliferation; cell shape; cell survival; culture technique; cytology; drug effect; fibroblast; flow cytometry; G1 phase cell cycle checkpoint; G2 phase cell cycle checkpoint; gingiva; human; M phase cell cycle checkpoint; metabolism; Apoptosis; Butyrates; cdc25 Phosphatases; Cell Culture Techniques; Cell Cycle; Cell Proliferation; Cell Shape; Cell Survival; Coloring Agents; Cyclin B; Cyclin B1; Fibroblasts; Flow Cytometry; Fluorescein-5-isothiocyanate; Fluoresceins; Fluorescent Dyes; G0 Phase; G1 Phase Cell Cycle Checkpoints; G2 Phase Cell Cycle Checkpoints; Gingiva; Humans; M Phase Cell Cycle Checkpoints; Propidium; Reactive Oxygen Species
|Appears in Collections:||臨床牙醫學研究所|
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