Role of calcineurin in Porphyromonas gingivalis-induced myocardial cell hypertrophy and apoptosis
Role of calcineurin in Porphyromonas gingivalis-induced myocardial cell hypertrophy and apoptosis
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DOI：
10.1007/s11373-005-9048-4
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发表时间：
2006-03-01
影响因子：
11
通讯作者：
Huang, CY
中科院分区：
文献类型：
--
作者：
Lee, SD;Kuo, WW;Huang, CY
背景与目的：牙周病原体牙龈卟啉单胞菌（P. gingivalis）增加心肌细胞肥大和凋亡，而放线菌杆菌和中间普雷沃氏菌对心肌细胞无影响。本研究旨在阐明钙调磷酸酶信号通路在牙龈卟啉诱导的H9c2心肌细胞肥大和凋亡中的作用。方法：采用琼脂糖凝胶电泳、DAPI、免疫荧光和Western blotting检测培养H9c2心肌细胞中钙调磷酸酶蛋白、Bcl2相关死亡启动子（Bad）和活化T细胞核因子(NFAT)-3蛋白产物的DNA片段化、核凝聚、细胞形态。结果：牙龈卟啉菌不仅增加了钙调磷酸酶蛋白、NFAT-3蛋白产物和细胞肥大，而且增加了H9c2细胞的DNA片段化、核凝聚和Bad蛋白产物。CsA预处理后，牙龈假单胞菌H9c2细胞增大的细胞大小、DNA断裂、核凝聚和Bad均明显减少。结论：本研究提示牙龈假单胞菌可能激活钙调磷酸酶信号通路，进而导致培养H9c2心肌细胞肥大和死亡。
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.