Back to Search
Start Over
Butyrate induces reactive oxygen species production and affects cell cycle progression in human gingival fibroblasts.
- Source :
-
Journal of periodontal research [J Periodontal Res] 2013 Feb; Vol. 48 (1), pp. 66-73. Date of Electronic Publication: 2012 Jul 27. - Publication Year :
- 2013
-
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.<br />Material and Methods: Human GFs were exposed to various concentrations of butyrate (0.5-16 mm) for 24 h. 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.<br />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 (4-16 mm) in GFs. However, no marked apoptosis of GFs was noted in this experimental condition. Butyrate (> 2 mm) 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.<br />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.<br /> (© 2012 John Wiley & Sons A/S.)
- Subjects :
- Apoptosis drug effects
Butyrates toxicity
CDC2 Protein Kinase
Cell Culture Techniques
Cell Cycle drug effects
Cell Proliferation drug effects
Cell Shape drug effects
Cell Survival drug effects
Coloring Agents
Cyclin B drug effects
Cyclin B1 drug effects
Cyclin-Dependent Kinases
Fibroblasts cytology
Flow Cytometry
Fluorescein-5-isothiocyanate
Fluoresceins
Fluorescent Dyes
G1 Phase Cell Cycle Checkpoints drug effects
G2 Phase Cell Cycle Checkpoints drug effects
Gingiva cytology
Humans
M Phase Cell Cycle Checkpoints drug effects
Propidium
Resting Phase, Cell Cycle drug effects
cdc25 Phosphatases drug effects
Butyrates pharmacology
Fibroblasts drug effects
Gingiva drug effects
Reactive Oxygen Species metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 1600-0765
- Volume :
- 48
- Issue :
- 1
- Database :
- MEDLINE
- Journal :
- Journal of periodontal research
- Publication Type :
- Academic Journal
- Accession number :
- 22834967
- Full Text :
- https://doi.org/10.1111/j.1600-0765.2012.01504.x