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p53-Pathway activity and apoptosis in hydrogen sulfide-exposed stem cells separated from human gingival epithelium.
MedLine Citation:
PMID:  23030661     Owner:  NLM     Status:  Publisher    
BACKGROUND AND OBJECTIVE: Hydrogen sulfide ( H(2) S ) is a volatile sulfur compound responsible for physiological halitosis. H(2) S was also reported as having periodontal pathologic activities. Gingival crevicular epithelium is the first barrier against periodontal pathogens and their products; oral keratinocyte stem cells OKSCs play key roles in maintaining this barrier. The p53 pathway is responsible for regulating key biological events. Increased apoptosis and cell-cycle arrest of DNA repair can affect keratinocyte stem cells, having a direct impact on the architecture of the oral epithelial tissue. However, the link between H(2) S , p53 activity and OKSCs has not yet been fully explored. The main objective of the present study was to explore the implications of the p53 pathway in OKSCs following exposure to H(2) S . MATERIAL AND METHODS: OKSCs were isolated from human gingival epithelium and incubated with physiological levels of H(2) S for 24 and 48 h. Apoptosis and the mitochondrial membrane potential were detected using flow cytometry. Cytochrome c, total p53, phosphorylated p53 and caspase activity were assessed using specific ELISAs. p53 Pathway gene activity was assayed using quantitative RT-PCR. RESULTS: The levels of apoptosis were significantly increased following incubation in the presence of H(2) S, especially after 48 h (36.95 ± 1.91% vs. 4.77 ± 0.74%). Caspases 9 and 3 were activated, whereas caspase-8 activity remained low. Total p53 activity and particularly phosphorylated p53 at serine 46, were significantly enhanced compared with controls (47.11 ± 9.84 units/mL vs. 0.15 ± 0 units/mL and 32.22 ± 10.23 units/mL  vs. 0.15 ± 0 units/mL, respectively, at 48 h). Among p53 pathway genes, apoptosis-related genes [i.e. phosphatase and tensin homolog ( PTEN ), B-cell CLL/lymphoma 2 ( BCL2), sirtuin 3 ( SIRT3) and caspases]) were dramatically increased when compared with controls. Moreover, cell-cycle progression genes [i.e. E2F transcription factor (E2F) family and histone deacetylase ( HDAC )] and DNA-repair genes [i.e. growth arrest and DNA-damage-inducible, gamma ( GADD45G ) family and serine/threonine-protein kinase Chk2 ( CHEK2)] were also increased. CONCLUSION: Following incubation with H(2) S , OKSCs express multiple p53-associated genes, including programmed cell death, cell-cycle control and DNA-repair genes.
B Calenic; K Yaegaki; N Ishkitiev; Y Kumazawa; T Imai; T Tanaka
Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2012-10-3
Journal Detail:
Title:  Journal of periodontal research     Volume:  -     ISSN:  1600-0765     ISO Abbreviation:  J. Periodont. Res.     Publication Date:  2012 Oct 
Date Detail:
Created Date:  2012-10-3     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.
Department of Oral Health, Nippon Dental University, Tokyo, Japan; Department of Biochemistry, Faculty of Dental Medicine, University of Medicine and Pharmacy "Carol Davila", Bucharest, Romania.
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