| Sign In to gain access to subscriptions and/or personal tools. |
Anti-proliferative Capsular-like Polysaccharide Antigen from Actinobacillus actinomycetemcomitans Induces Apoptotic Cell Death in Mouse Osteoblastic MC3T3-E1 CellsDepartment of Periodontology, School of Dentistry, Aichi-Gakuin University, Nagoya 464-8650, Japan
Department of Pharmacology, School of Dentistry, Aichi-Gakuin University, Nagoya 464-8650, Japan
Department of Pharmacology, School of Dentistry, Aichi-Gakuin University, Nagoya 464-8650, Japan
Department of Periodontology, School of Dentistry, Aichi-Gakuin University, Nagoya 464-8650, Japan
Department of Periodontology, School of Dentistry, Aichi-Gakuin University, Nagoya 464-8650, Japan
Department of Periodontology, School of Dentistry, Aichi-Gakuin University, Nagoya 464-8650, Japan
Department of Oral Science, The National Institute of Infectious Diseases, Tokyo 162-8640, Japan
Department of Periodontology, School of Dentistry, Aichi-Gakuin University, Nagoya 464-8650, Japan
Department of Pharmacology, School of Dentistry, Aichi-Gakuin University, Nagoya 464-8650, Japan
Actinobacillus actinomycetemcomitans (A. actinomycetemcomitans) has been implicated in the etiology of localized juvenile periodontitis (LJP), and produces a multiplicity of tissue-damaging products. Among those products, the capsular-like polysaccharide antigen (CPA) from A. actinomycetemcomitans is a potent mediator of bone resorption. In fact, this CPA (serotype b) is known to promote osteoclast-like cell formation via interleukin (IL)-1
Key Words: A. actinomycetemcomitans, apoptosis • DNA fragmentation • MC3T3-E1 • SaOS-2
Journal of Dental Research, Vol. 78, No. 6,
1230-1237 (1999) This article has been cited by other articles:
|
||||||||||||||||||||||||||||
 |
|
|
 |
|
Sign In to gain access to subscriptions and/or personal tools.
production in mouse marrow cultures. Although osteoblasts complete bone formation, there are few reports focusing on the effect of CPA in bone-forming activity of osteoblasts in inflammatory disease sites. We hypothesized that CPA plays a mediating role in osteoblastic cells. Therefore, the purpose of this study was to examine the effect of CPA from A. actinomycetemcomitans on the mouse osteoblastic cell line MC3T3-E1 and human osteosarcoma SaOS-2 cells. A. actinomycetemcomitans serotype c resulted in a potent dose-dependent inhibition of cell proliferation of both cell lines. Characterization of the antiproliferative activity in the CPA demonstrated that it was not cytotoxic for MC3T3-El. A 20-hour incubation with CPA-c resulted in a significant increase in apoptotic cell death in the cells, as evaluated by both cellular DNA fragmentation ELISA and FACS analysis. In contrast to the results obtained with a cytokine mixture (tumor necrosis factor-
), no inducible nitric oxide (NO) synthase gene expression or NO release could be detected in MC3T3-E1 after incubation with CPA-c. Further, both CPA-b and -c caused potent induction of apoptosis-related modifiers, e.g., Fas mRNA, whereas bcl-2 mRNA levels were unchanged. Therefore, this study has shown that CPA from A. actinomycetemcomitans contains a potent antiproliferative polysaccharide whose activity is associated with apoptotic cell death in MC3T3-E1, and that CPA per se is an inducer of apoptosis mediated by the Fas system but not by NO. 
