Possible involvement of protein kinase C in apoptotic cell death of macrophages infected with Actinobacillus actinomycetemcomitans
Koji Nonaka
Department of Oral Science, National Institute of Infectious Diseases, 1-23-1 Toyama, Shinjuku-ku, Tokyo 162, Japan
Department of Periodontology, School of Dentistry, Health Sciences University of Hokkaido, Hokkaido 061-02, Japan
Search for more papers by this authorAkira Ishisaki
Department of Oral Science, National Institute of Infectious Diseases, 1-23-1 Toyama, Shinjuku-ku, Tokyo 162, Japan
Search for more papers by this authorMiyuki Muro
Department of Periodontology, School of Dentistry, Health Sciences University of Hokkaido, Hokkaido 061-02, Japan
Search for more papers by this authorSatsuki Kato
Department of Periodontology, School of Dentistry, Health Sciences University of Hokkaido, Hokkaido 061-02, Japan
Search for more papers by this authorMari Oido
Department of Periodontology, School of Dentistry, Health Sciences University of Hokkaido, Hokkaido 061-02, Japan
Search for more papers by this authorKeisuke Nakashima
Department of Periodontology, School of Dentistry, Health Sciences University of Hokkaido, Hokkaido 061-02, Japan
Search for more papers by this authorYusuke Kowashi
Department of Periodontology, School of Dentistry, Health Sciences University of Hokkaido, Hokkaido 061-02, Japan
Search for more papers by this authorCorresponding Author
Tatsuji Nishihara
Department of Oral Science, National Institute of Infectious Diseases, 1-23-1 Toyama, Shinjuku-ku, Tokyo 162, Japan
*Corresponding author. Tel.: (81) (3) 5285-1111; Fax: (81) (3) 5285-1172; E-mail: [email protected]Search for more papers by this authorKoji Nonaka
Department of Oral Science, National Institute of Infectious Diseases, 1-23-1 Toyama, Shinjuku-ku, Tokyo 162, Japan
Department of Periodontology, School of Dentistry, Health Sciences University of Hokkaido, Hokkaido 061-02, Japan
Search for more papers by this authorAkira Ishisaki
Department of Oral Science, National Institute of Infectious Diseases, 1-23-1 Toyama, Shinjuku-ku, Tokyo 162, Japan
Search for more papers by this authorMiyuki Muro
Department of Periodontology, School of Dentistry, Health Sciences University of Hokkaido, Hokkaido 061-02, Japan
Search for more papers by this authorSatsuki Kato
Department of Periodontology, School of Dentistry, Health Sciences University of Hokkaido, Hokkaido 061-02, Japan
Search for more papers by this authorMari Oido
Department of Periodontology, School of Dentistry, Health Sciences University of Hokkaido, Hokkaido 061-02, Japan
Search for more papers by this authorKeisuke Nakashima
Department of Periodontology, School of Dentistry, Health Sciences University of Hokkaido, Hokkaido 061-02, Japan
Search for more papers by this authorYusuke Kowashi
Department of Periodontology, School of Dentistry, Health Sciences University of Hokkaido, Hokkaido 061-02, Japan
Search for more papers by this authorCorresponding Author
Tatsuji Nishihara
Department of Oral Science, National Institute of Infectious Diseases, 1-23-1 Toyama, Shinjuku-ku, Tokyo 162, Japan
*Corresponding author. Tel.: (81) (3) 5285-1111; Fax: (81) (3) 5285-1172; E-mail: [email protected]Search for more papers by this authorAbstract
We have previously reported the evidence for apoptosis in the mouse macrophage cell line J774.1 by the periodontopathic bacterium Actinobacillus actinomycetemcomitans. In this study, we examined the role of protein kinases in the induction of apoptosis in A. actinomycetemcomitans-infected J774.1 cells by the MTT assay, fluorescence microscopy and flow cytometric analysis. After J774.1 cells were precultured with protein kinase C (PKC) activator, phorbol 12-myristate 13-acetate (PMA), J774.1 cells infected with A. actinomycetemcomitans showed the increased percentage of apoptotic cells. On the contrary, protein kinase A (PKA) activators, such as forskolin and dibutyryl cAMP, do not mimic the effect of PMA. PKC inhibitors, such as staurosporine, calphostin C, chelerythrine chloride, and H7 were found to suppress apoptotic cell death in J774.1 cells infected with A. actinomycetemcomitans. However, HA1004, known as PKA inhibitor, had no effect on apoptosis in infected macrophages. The results presented here suggest that the signals through PKC may play crucial roles in the modulation of apoptosis in macrophages infected with A. actinomycetemcomitans.
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