Page 102 - Read Online
P. 102

Page 16 of 18                                                 Kozarov et al. Vessel Plus 2020;4:10  I  http://dx.doi.org/10.20517/2574-1209.2019.31

                   2000 2000;24:153-92.
               87.  Potempa J, Sroka A, Imamura T, Travis J. Gingipains, the major cysteine proteinases and virulence factors of Porphyromonas
                   gingivalis: structure, function and assembly of multidomain protein complexes. Curr Protein Pept Sci 2003;4:397-407.
               88.  Travis J, Banbula A, Potempa J. The role of bacterial and host proteinases in periodontal disease. Adv Exp Med Biol 2000;477:455-65.
               89.  Johansson A, Kalfas S. Characterization of the proteinase-dependent cytotoxicity of Porphyromonas gingivalis. Eur J Oral Sci
                   1998;106:863-71.
               90.  Chen T, Nakayama K, Belliveau L, Duncan MJ. Porphyromonas gingivalis gingipains and adhesion to epithelial cells. Infect Immun
                   2001;69:3048-56.
               91.  Roth GA, Ankersmit HJ, Brown VB, Papapanou PN, Schmidt AM, et al. Porphyromonas gingivalis infection and cell death in human
                   aortic endothelial cells. FEMS Microbiol Lett 2007;272:106-13.
               92.  Hirasawa M, Kurita-Ochiai T. Porphyromonas gingivalis induces apoptosis and autophagy via ER stress in human umbilical vein
                   endothelial cells. Mediators Inflamm 2018;2018:1967506.
               93.  Pham K, Feik D, Hammond BF, Rams TE, Whitaker EJ. Aggregation of human platelets by gingipain-R from Porphyromonas
                   gingivalis cells and membrane vesicles. Platelets 2002;13:21-30.
               94.  Lourbakos A, Yuan YP, Jenkins AL, Travis J, Andrade-Gordon P, et al. Activation of protease-activated receptors by gingipains from
                   Porphyromonas gingivalis leads to platelet aggregation: a new trait in microbial pathogenicity. Blood 2001;97:3790-7.
               95.  Arvanitidis E, Bizzarro S, Alvarez Rodriguez E, Loos BG, Nicu EA. Reduced platelet hyper-reactivity and platelet-leukocyte
                   aggregation after periodontal therapy. Thromb J 2017;15:5.
               96.  Klarström Engström K, Khalaf H, Kälvegren H, Bengtsson T. The role of Porphyromonas gingivalis gingipains in platelet activation
                   and innate immune modulation. Mol Oral Microbiol 2015;30:62-73.
               97.  Lönn J, Ljunggren S, Klarström-Engström K, Demirel I, Bengtsson T, et al. Lipoprotein modifications by gingipains of
                   Porphyromonas gingivalis. J Periodontal Res 2018;53:403-13.
               98.  Joo JY, Cha GS, Chung J, Lee JY, Kim SJ, et al. Peptide 19 of porphyromonas gingivalis heat shock protein is a potent inducer of low-
                   density lipoprotein oxidation. J Periodontol 2017;88:e58-e64.
               99.  Wallet SM, Puri V, Gibson FC. Linkage of infection to adverse systemic complications: periodontal disease, toll-like receptors, and
                   other pattern recognition systems. Vaccines (Basel) 2018;6:21.
               100.  Hernández-Ríos P, Pussinen PJ, Vernal R, Hernández M. Oxidative stress in the local and systemic events of apical periodontitis. Front
                   Physiol 2017;8:869.
               101.  Sessa R, Pietro MD, Filardo S, Turriziani O. Infectious burden and atherosclerosis: a clinical issue. World J Clin Cases 2014;2:240-9.
               102.  He F, Zuo L. Redox roles of reactive oxygen species in cardiovascular diseases. Int J Mol Sci 2015;16:27770-80.
               103.  Di Pietro M, Filardo S, Falasca F, Turriziani O, Sessa R. Infectious agents in atherosclerotic cardiovascular diseases through oxidative
                   stress. Int J Mol Sci 2017;18:2459.
               104.  Förstermann U, Xia N, Li H. Roles of vascular oxidative stress and nitric oxide in the pathogenesis of atherosclerosis. Circ Res
                   2017;120:713-35.
               105.  Li L, Michel R, Cohen J, Decarlo A, Kozarov E. Intracellular survival and vascular cell-to-cell transmission of Porphyromonas
                   gingivalis. BMC Microbiol 2008;8:26.
               106.  Azenabor AA, Yang S, Job G, Adedokun OO. Elicitation of reactive oxygen species in Chlamydia pneumoniae-stimulated
                   macrophages: a Ca2+-dependent process involving simultaneous activation of NADPH oxidase and cytochrome oxidase genes. Med
                   Microbiol Immunol 2005;194:91-103.
               107.  Di Pietro M, Filardo S, De Santis F, Sessa R. Chlamydia pneumoniae infection in atherosclerotic lesion development through oxidative
                   stress: a brief overview. Int J Mol Sci 2013;14:15105-20.
               108.  Yamaguchi Y, Kurita-Ochiai T, Kobayashi R, Suzuki T, Ando T. Activation of the NLRP3 inflammasome in Porphyromonas
                   gingivalis-accelerated atherosclerosis. Pathog Dis 2015;73:ftv011.
               109.  Li XY, Wang C, Xiang XR, Chen FC, Yang CM, et al. Porphyromonas gingivalis lipopolysaccharide increases lipid accumulation by
                   affecting CD36 and ATP-binding cassette transporter A1 in macrophages. Oncol Rep 2013;30:1329-36.
               110.  Pollreisz A, Huang Y, Roth GA, Cheng B, Kebschull M, et al. Enhanced monocyte migration and pro-inflammatory cytokine
                   production by Porphyromonas gingivalis infection. J Periodontal Res 2010;45:239-45.
               111.  Sheets SM, Potempa J, Travis J, Casiano CA, Fletcher HM. Gingipains from Porphyromonas gingivalis W83 induce cell adhesion
                   molecule cleavage and apoptosis in endothelial cells. Infect Immun 2005;73:1543-52.
               112.  Bugueno IM, Khelif Y, Seelam N, Morand DN, Tenenbaum H, et al. Porphyromonas gingivalis differentially modulates cell death
                   profile in Ox-LDL and TNF-α pre-treated endothelial cells. PLoS One 2016;11:e0154590.
               113.  Shiheido Y, Maejima Y, Suzuki JI, Aoyama N, Kaneko M, et al. Porphyromonas gingivalis, a periodontal pathogen, enhances
                   myocardial vulnerability, thereby promoting post-infarct cardiac rupture. J Mol Cell Cardiol 2016;99:123-37.
               114.  Amberger A, Maczek C, Jürgens G, Michaelis D, Schett G, et al. Co-expression of ICAM-1, VCAM-1, ELAM-1 and Hsp60 in human
                   arterial and venous endothelial cells in response to cytokines and oxidized low-density lipoproteins. Cell Stress Chaperones 1997;2:94-103.
               115.  Takei A, Huang Y, Lopes-Virella MF. Expression of adhesion molecules by human endothelial cells exposed to oxidized low density
                   lipoprotein. Influences of degree of oxidation and location of oxidized LDL. Atherosclerosis 2001;154:79-86.
               116.  Malekmohammad K, Sewell RDE, Rafieian-Kopaei M. Antioxidants and atherosclerosis: mechanistic aspects. Biomolecules
                   2019;9:301.
               117.  Hulsmans M, Holvoet P. The vicious circle between oxidative stress and inflammation in atherosclerosis. J Cell Mol Med 2010;14:70-8.
   97   98   99   100   101   102   103   104   105   106   107