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|標題:||Role of calcineurin in Porphyromonas gingivalis-induced myocardial cell hypertrophy and apoptosis||作者:||Lee, S.D.
|關鍵字:||periodontitis;Porphyromonas gingivalis;myocardial cell;apoptotic;cell death;calcineurin signal pathways;cardiac-hypertrophy;heart-failure;therapeutic target;activation;pathway;expression||Project:||Journal of Biomedical Science||期刊/報告no：:||Journal of Biomedical Science, Volume 13, Issue 2, Page(s) 251-260.||摘要:||
Background and objective: Periodontal pathogen Porphyromonas gingivalis (P. gingivalis) increased cardiomyocyte hypertrophy and apoptosis whereas Actinobaeillus actinomycetemcomitans and Prevotella intermedia had no effects. The purpose of this study is to clarify the role of calcineurin signaling pathway in P. gingivalis-induced H9c2 myocardial cell hypertrophy and apoptosis. Methods: DNA fragmentation, nuclear condensation, cellular morphology, calcineurin protein, Bcl2- associated death promoter (Bad) and nuclear factor of activated T cell (NFAT)-3 protein products in cultured H9c2 myocardial cell were measured by agarose gel electrophoresis, DAPI, immunofluorescence, and Western blotting following P. gingivalis and/or pre-administration of CsA (calcineurin inhibitors cyclosporin A). Results: P. gingivalis not only increased calcineurin protein, NFAT-3 protein products and cellular hypertrophy, but also increased DNA fragmentation, nuclear condensation and Bad protein products in H9c2 cells. The increased cellular sizes, DNA fragmentation, nuclear condensation, and Bad of H9c2 cells treated with P. gingivalis were all significantly reduced after pre-administration of CsA. Conclusion: Our findings suggest that the activity of calcineurin signal pathway may be initiated by P. gingivalis and further lead to cell hypertrophy and death in culture H9c2 myocardial cells.
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