Toll-like receptor 4 signaling has a critical role in Porphyromonas gingivalis-accelerated neointimal formation after arterial injury in mice
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Y. Izumi | I. Komuro | Hiroki Sato | M. Isobe | H. Akazawa | J. Suzuki | N. Aoyama | Yuichi Ikeda | N. Kobayashi | H. Kumagai | Kouji Wakayama | Shouta Akimoto | Hiroki Sato
[1] Jingsheng Guo,et al. Interleukin-1 Receptor-Associated Kinase 1/4 as a Novel Target for Inhibiting Neointimal Formation After Carotid Balloon Injury. , 2015, Journal of atherosclerosis and thrombosis.
[2] M. Matsuzaki,et al. TLR4 is a critical regulator of angiotensin II-induced vascular remodeling: the roles of extracellular SOD and NADPH oxidase , 2015, Hypertension Research.
[3] L. Kesavalu,et al. Myxomavirus Anti-Inflammatory Chemokine Binding Protein Reduces the Increased Plaque Growth Induced by Chronic Porphyromonas gingivalis Oral Infection after Balloon Angioplasty Aortic Injury in Mice , 2014, PloS one.
[4] H. Itoh,et al. Significant roles of the (pro)renin receptor in integrity of vascular smooth muscle cells , 2014, Hypertension Research.
[5] Y. Izumi,et al. Porphyromonas gingivalis promotes neointimal formation after arterial injury through toll-like receptor 2 signaling , 2014, Heart and Vessels.
[6] Y. Pi,et al. Inhibition of reactive oxygen species generation attenuates TLR4-mediated proinflammatory and proliferative phenotype of vascular smooth muscle cells , 2013, Laboratory Investigation.
[7] Cun-Yu Wang,et al. Tetra- and Penta-Acylated Lipid A Structures of Porphyromonas gingivalis LPS Differentially Activate TLR4-Mediated NF-κB Signal Transduction Cascade and Immuno-Inflammatory Response in Human Gingival Fibroblasts , 2013, PloS one.
[8] Y. Izumi,et al. Porphyromonas gingivalis Accelerates Neointimal Formation after Arterial Injury , 2012, Journal of Vascular Research.
[9] A. Progulske-Fox,et al. Both the unique and repeat regions of the Porphyromonas gingivalis hemagglutin A are involved in adhesion and invasion of host cells. , 2012, Anaerobe.
[10] Jing Xiang,et al. PPARγ attenuates intimal hyperplasia by inhibiting TLR4-mediated inflammation in vascular smooth muscle cells. , 2011, Cardiovascular research.
[11] S. Akira,et al. Toll-like receptors and their crosstalk with other innate receptors in infection and immunity. , 2011, Immunity.
[12] Zhi-yong Chen,et al. The periodontal anaerobe Porphyromonas gingivalis induced platelet activation and increased aggregation in whole blood by rat model. , 2011, Thrombosis research.
[13] D. Grenier,et al. Proteases of Porphyromonas gingivalis as important virulence factors in periodontal disease and potential targets for plant-derived compounds: a review article. , 2011, Current drug targets.
[14] X. Liu,et al. Pathogen-Mediated Inflammatory Atherosclerosis Is Mediated in Part via Toll-Like Receptor 2-Induced Inflammatory Responses , 2010, Journal of Innate Immunity.
[15] Y. Taniyama,et al. Ultrasound-microbubble-mediated intercellular adhesion molecule-1 small interfering ribonucleic acid transfection attenuates neointimal formation after arterial injury in mice. , 2010, Journal of the American College of Cardiology.
[16] 増田 隆宏. Mouse macrophages primed with alendronate down-regulate monocyte chemoattractant protein-1 (MCP-1) and macrophage inflammatory protein-1alpha (MIP-1alpha) production in response to Toll-like receptor (TLR) 2 and TLR4 agonist , 2009 .
[17] R. Nagai,et al. Fluvastatin accelerates re-endothelialization impaired by local sirolimus treatment. , 2009, European journal of pharmacology.
[18] AndreasSchober. Chemokines in Vascular Dysfunction and Remodeling , 2008 .
[19] A. Itai,et al. The effects of pharmacological PAI-1 inhibition on thrombus formation and neointima formation after arterial injury , 2008, Expert opinion on therapeutic targets.
[20] K. Chayama,et al. Role of the Angiotensin II Type 2 Receptor in Arterial Remodeling after Wire Injury in Mice , 2008, Hypertension Research.
[21] F. C. Gibson,et al. Sensitization of Human Aortic Endothelial Cells to Lipopolysaccharide via Regulation of Toll-Like Receptor 4 by Bacterial Fimbria-Dependent Invasion , 2005, Infection and Immunity.
[22] Y. Taniyama,et al. Ultrasound-Microbubble-Mediated NF-κB Decoy Transfection Attenuates Neointimal Formation after Arterial Injury in Mice , 2005, Journal of Vascular Research.
[23] F. C. Gibson,et al. Innate Immune Recognition of Invasive Bacteria Accelerates Atherosclerosis in Apolipoprotein E–Deficient Mice , 2004, Circulation.
[24] H. Matsubara,et al. Bone Marrow Monocyte Lineage Cells Adhere on Injured Endothelium in a Monocyte Chemoattractant Protein-1–Dependent Manner and Accelerate Reendothelialization as Endothelial Progenitor Cells , 2003, Circulation research.
[25] M. M. Cowan,et al. Virulence factors of Porphyromonas gingivalis are modified by polyphenol oxidase and asparaginase. , 2003, Oral microbiology and immunology.
[26] U. Kalnins,et al. Heparin-Coated Stent Placement for the Treatment of Stenoses in Small Coronary Arteries of Symptomatic Patients , 2003, Circulation.
[27] F. Van de Werf,et al. Chlamydia pneumoniae induces neointima formation in coronary arteries of normal pigs. , 2003, Cardiovascular research.
[28] S. Socransky,et al. Subgingival microbial profiles in refractory periodontal disease. , 2002, Journal of clinical periodontology.
[29] K. Ohura,et al. Porphyromonas gingivalis lipopolysaccharide signaling in gingival fibroblasts-CD14 and Toll-like receptors. , 2002, Critical reviews in oral biology and medicine : an official publication of the American Association of Oral Biologists.
[30] E. L. Batista,et al. Porphyromonas gingivalis Infection Accelerates the Progression of Atherosclerosis in a Heterozygous Apolipoprotein E–Deficient Murine Model , 2002, Circulation.
[31] S. Hokimoto,et al. Plasma monocyte chemoattractant protein-1 antigen levels and the risk of restenosis after coronary stent implantation. , 2001, Japanese circulation journal.
[32] M. Makuuchi,et al. A mouse model of vascular injury that induces rapid onset of medial cell apoptosis followed by reproducible neointimal hyperplasia. , 2000, Journal of molecular and cellular cardiology.
[33] M. Trevisan,et al. Identification of periodontal pathogens in atheromatous plaques. , 2000, Journal of periodontology.
[34] H. Pahl. Activators and target genes of Rel/NF-κB transcription factors , 1999, Oncogene.
[35] KohOno,et al. Anti–Monocyte Chemoattractant Protein-1/Monocyte Chemotactic and Activating Factor Antibody Inhibits Neointimal Hyperplasia in Injured Rat Carotid Arteries , 1999 .
[36] P. Vokonas,et al. An association between periodontal disease and peripheral vascular disease. , 1998, American journal of surgery.
[37] T. Warner,et al. Monocyte chemotactic protein-1 expression is associated with the development of vein graft intimal hyperplasia. , 1997, Arteriosclerosis, thrombosis, and vascular biology.
[38] I. Ishikawa,et al. Relationship between serum antibody levels and subgingival colonization of Porphyromonas gingivalis in patients with various types of periodontitis. , 1997, Journal of periodontology.
[39] A. Takeshita,et al. CD14-mediated signal pathway of Porphyromonas gingivalis lipopolysaccharide in human gingival fibroblasts , 1996, Infection and immunity.
[40] A. Itai,et al. The effects of pharmacological PAI-1 inhibition on thrombus formation and neointima formation after arterial injury. , 2008, Expert opinion on therapeutic targets.
[41] 稲垣 裕. Ultrasound-microbubble-mediated NF-κB decoy transfection attenuates neointimal formation after arterial injury in mice , 2008 .
[42] E. Lien,et al. Toll-like receptors. , 2002, Critical care medicine.
[43] H. Pahl,et al. Activators and target genes of Rel/NF-kappaB transcription factors. , 1999, Oncogene.