Document Detail

Butyrate induces reactive oxygen species production and affects cell cycle progression in human gingival fibroblasts.
MedLine Citation:
PMID:  22834967     Owner:  NLM     Status:  Publisher    
Chang MC, Tsai YL, Chen YW, Chan CP, Huang CF, Lan WC, Lin CC, Lan WH, Jeng JH. Butyrate induces reactive oxygen species production and affects cell cycle progression in human gingival fibroblasts. J Periodont Res 2012; doi: 10.1111/j.1600-0765.2012.01504.x. © 2012 John Wiley & Sons A/S 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 (0.5-16 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. 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. 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.
M-C Chang; Y-L Tsai; Y-W Chen; C-P Chan; C-F Huang; W-C Lan; C-C Lin; W-H Lan; J-H Jeng
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2012-7-27
Journal Detail:
Title:  Journal of periodontal research     Volume:  -     ISSN:  1600-0765     ISO Abbreviation:  -     Publication Date:  2012 Jul 
Date Detail:
Created Date:  2012-7-27     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0055107     Medline TA:  J Periodontal Res     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
© 2012 John Wiley & Sons A/S.
Biomedical Science Team, Chang Gung University of Science and Technology, Taoyuan, Taiwan Graduate Institute of Clinical Dentistry and Department of Dentistry, National Taiwan University Hospital and National Taiwan University Medical College, Taipei, Taiwan Department of Dentistry, Chang Gung Memorial Hospital, Taipei, Taiwan Department of Dentistry, Taipei Medical University Hospital, Taipei, Taiwan Department of Dentistry, Chang Gung Memorial Hospital, Kaohsiung, Taiwan.
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