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Proliferation of Smooth Muscle Cells Stimulated by Porphyromonas Gingivalis is Inhibited by Apple Polyphenol
Author(s) -
Inaba Hiroaki,
Tagashira Motoyuki,
Kanda Tomomasa,
Amano Atsuo
Publication year - 2011
Publication title -
journal of periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.036
H-Index - 156
eISSN - 1943-3670
pISSN - 0022-3492
DOI - 10.1902/jop.2011.100785
Subject(s) - porphyromonas gingivalis , polyphenol , smooth muscle , chemistry , microbiology and biotechnology , biology , periodontitis , dentistry , medicine , biochemistry , endocrinology , antioxidant
Background: Porphyromonas gingivalis ( Pg ) is thought to be involved in the progression of occlusive arterial lesions, whereas vascular smooth muscle cell (SMC) proliferation is considered to be involved in occlusive arterial disease. We previously showed that bacteremia caused by Pg infection induced proliferation of mouse aortic SMCs. Furthermore, human SMCs stimulated with human plasma incubated with Pg showed a marked transformation from the contractile to proliferative phenotype. In the present study, we examine the involvement of Pg gingipains and fimbriae in induction of the SMC transformation and proliferation, and effective inhibitors. Methods: Pg strains including gingipain‐ and fimbria‐null mutants were incubated in human plasma, after which the bacteria were removed and the supernatants were added to cultured SMCs. To evaluate the effects of inhibitors, Pg organisms were incubated in plasma in the presence of apple polyphenol (AP), epigallocatechin gallate, KYT‐1 (Arg‐gingipain inhibitor), and KYT‐36 (Lys‐gingipain inhibitor). Results: Plasma supernatants from wild‐type and fimbria‐mutant cultures markedly stimulated cellular proliferation, whereas those containing gingipain‐null mutants showed negligible effects. SMC proliferation was also induced by plasma treated with trypsin. Furthermore, plasma supernatants cultured in the presence of KYT‐1/KYT‐36 and AP showed significant inhibitory effects on SMC proliferation, whereas cultures with epigallocatechin gallate did not. Conclusion: Our results suggest that Pg gingipains are involved in the induction of SMC transformation and proliferation, whereas this was inhibited by AP.