首页> 外文期刊>Journal of pharmacological sciences. >Roles of Oral Bacteria in Cardiovascular Diseases — From Molecular Mechanisms to Clinical Cases: Porphyromonas gingivalis Is the Important Role of Intimal Hyperplasia in the Aorta
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Roles of Oral Bacteria in Cardiovascular Diseases — From Molecular Mechanisms to Clinical Cases: Porphyromonas gingivalis Is the Important Role of Intimal Hyperplasia in the Aorta

机译:口腔细菌在心血管疾病中的作用-从分子机制到临床病例:牙龈卟啉单胞菌是主动脉内膜增生的重要作用

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References(9) Cited-By(10) It has been reported that DNA of oral bacterial species, such as Porphyromonas gingivalis and Streptococcus mutans, was detected frequently in specimens of arteriosclerotic vessels. However, the source of DNA, whether from live intact bacteria or a part of the bacteria, has not been identified yet. Moreover, there was no precise evidence concerning involvement of oral bacteria in the progression of arteriosclerosis. We tried to clarify the involvement of P. gingivalis on the mechanisms of development of aortic intimal hyperplasia. Intravenous administration of P. gingivalis dramatically induced intimal hyperplasia in the mouse model with photochemical impairment of the femoral artery. However there were no changes identified in the mice without aortic impairment, even with the P. gingivalis infection. Concomitantly, S100 calcium–binding protein A9 (S100A9) and the embryonic isoform of myosin heavy chain (SMemb), a proliferative phenotypic marker of smooth muscle cells, were significantly overexpressed on the surfaces of smooth muscle cells present in the injured blood vessels. Similarly, increased expressions of S100A9 and SMemb proteins were observed in aneurismal specimens obtained from P. gingivalis–infected patients. We found that bacteremia induced by P. gingivalis leads to intimal hyperplasia associated with overexpressions of S100A9 and SMemb. Our results strongly suggest that oral-hematogenous spreading of P. gingivalis is a causative event in the development of aortic hyperplasia in periodontitis patients.
机译:参考文献(9)By-By(10)据报道,在动脉硬化血管样本中经常检测到口腔细菌物种的DNA,例如牙龈卟啉单胞菌和变形链球菌。但是,DNA的来源,无论是活的完整细菌还是细菌的一部分,都尚未被发现。而且,没有确切的证据表明口腔细菌参与了动脉硬化的发展。我们试图阐明牙龈卟啉单胞菌与主动脉内膜增生发生机制的关系。静脉注射牙龈卟啉单胞菌可在小鼠模型中引起内膜增生,并伴有股动脉的光化学损伤。但是,即使有牙龈卟啉单胞菌感染,在没有主动脉损伤的小鼠中也没有发现变化。同时,S100钙结合蛋白A9(S100A9)和平滑肌细胞增殖表型标志物肌球蛋白重链的胚胎同工型(SMemb)在受伤血管中存在的平滑肌细胞表面上明显过表达。同样,从牙龈卟啉单胞菌感染患者获得的动脉瘤标本中观察到S100A9和SMemb蛋白的表达增加。我们发现由牙龈卟啉单胞菌诱导的菌血症导致与S100A9和SMemb的过表达相关的内膜增生。我们的结果有力地表明,牙龈卟啉单胞菌的口腔血行性扩散是牙周炎患者主动脉增生发展的原因。

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