Synergic induction of human periodontal ligament fibroblast cell death by nitric oxide and N-methyl-D-aspartic acid receptor antagonist.
10.5051/jpis.2011.41.1.17
- Author:
Taegun SEO
1
;
Seho CHA
;
Kyung Mi WOO
;
Yun Soo PARK
;
Yun Mi CHO
;
Jeong Soon LEE
;
Tae Il KIM
Author Information
1. Department of Life Science, Dongguk University-Seoul, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Cell proliferation;
Mitogen-activated protein kinase;
N-methyl-D-aspartate receptor;
Periodontal ligament
- MeSH:
Apoptosis;
Blotting, Western;
Caspase 3;
Cell Count;
Cell Death;
Cell Proliferation;
Cell Survival;
Culture Media;
Cytochromes c;
Dizocilpine Maleate;
Fibroblasts;
Humans;
Hydrogen;
Maleates;
N-Methylaspartate;
Nitric Oxide;
Nitroprusside;
Osteoblasts;
Periodontal Ligament;
Protein Kinases;
Proteins;
Tissue Donors
- From:Journal of Periodontal & Implant Science
2011;41(1):17-22
- CountryRepublic of Korea
- Language:English
-
Abstract:
PURPOSE: Nitric oxide (NO) has been known as an important regulator of osteoblasts and periodontal ligament cell activity. This study was performed to investigate the relationship between NO-mediated cell death of human periodontal ligament fibroblasts (PDLFs) and N-methyl-D-aspartic acid (NMDA) receptor antagonist (+)-5-methyl-10, 11-dihydro-5H-dibenzo[a,d]cyclohepten-5, 10-imine hydrogen maleate (MK801). METHODS: Human PDLFs were treated with various concentrations (0 to 4 mM) of sodium nitroprusside (SNP) with or without 200 microM MK801 in culture media for 16 hours and the cell medium was then removed and replaced by fresh medium containing MTS reagent for cell proliferation assay. Western blot analysis was performed to investigate the effects of SNP on the expression of Bax, cytochrome c, and caspase-3 proteins. The differences for each value among the sample groups were compared using analysis of variance with 95% confidence intervals. RESULTS: In the case of SNP treatment, as a NO donor, cell viability was significantly decreased in a concentration-dependent manner. In addition, a synergistic effect was shown when both SNP and NMDA receptor antagonist was added to the medium. SNP treated PDLFs exhibited a round shape in culture conditions and were dramatically reduced in cell number. SNP treatment also increased levels of apoptotic marker protein, such as Bax and cytochrome c, and reduced caspase-3 in PDLFs. Mitogen-activated protein kinase signaling was activated by treatment of SNP and NMDA receptor antagonist. CONCLUSIONS: These results suggest that excessive production of NO may induce apoptosis and that NMDA receptor may modulate NO-induced apoptosis in PDLFs.
