Association of matrix metalloproteinase (MMP-1, MMP-3 and MMP-9) and cyclooxygenase-2 gene polymorphisms and their proteins with chronic periodontitis

2011 ◽  
Vol 56 (10) ◽  
pp. 1081-1090 ◽  
Author(s):  
Wings T.Y. Loo ◽  
Min Wang ◽  
L.J. Jin ◽  
Mary N.B. Cheung ◽  
G.R. Li
2012 ◽  
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Anika Daing ◽  
Sarvendra Vikram Singh ◽  
Charanjeet Singh Saimbi ◽  
Mohammad Akhlaq Khan ◽  
Srikanta Kumar Rath

2008 ◽  
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Ali Gürkan ◽  
Gülnur Emingil ◽  
Buket Han Saygan ◽  
Gül Atilla ◽  
Serhat Çınarcık ◽  
...  

2012 ◽  
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pp. 188-196 ◽  
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B. Hrdlickova ◽  
J. Vokurka ◽  
A. Fassmann

2011 ◽  
Vol 56 (1) ◽  
pp. 54-62 ◽  
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Ana Paula de Souza Pardo ◽  
Raquel M. Scarel-Caminaga ◽  
Rui B. de Brito ◽  
Fabiano Alvim-Pereira ◽  
...  

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Daniel J. Sexton ◽  
...  

Background Abdominal aortic aneurysm (AAA) is an important cause of mortality in older adults. The kinin B2 receptor agonist, bradykinin, has been implicated in AAA pathogenesis through promoting inflammation. Bradykinin is generated from high‐ and low‐molecular‐weight kininogen by the serine protease kallikrein‐1. The aims of this study were first to examine the effect of neutralizing kallikrein‐1 on AAA development in a mouse model and second to test how blocking kallikrein‐1 affected cyclooxygenase‐2 and prostaglandin E 2 in human AAA explants. Methods and Results Neutralization of kallikrein‐1 in apolipoprotein E‐deficient ( ApoE −/− ) mice via administration of a blocking antibody inhibited suprarenal aorta expansion in response to angiotensin (Ang) II infusion. Kallikrein‐1 neutralization decreased suprarenal aorta concentrations of bradykinin and prostaglandin E 2 and reduced cyclooxygenase‐2 activity. Kallikrein‐1 neutralization also decreased protein kinase B and extracellular signal‐regulated kinase 1/2 phosphorylation and reduced levels of active matrix metalloproteinase 2 and matrix metalloproteinase 9. Kallikrein‐1 blocking antibody reduced levels of cyclooxygenase‐2 and secretion of prostaglandin E 2 and active matrix metalloproteinase 2 and matrix metalloproteinase 9 from human AAA explants and vascular smooth muscle cells exposed to activated neutrophils. Conclusions These findings suggest that kallikrein‐1 neutralization could be a treatment target for AAA.


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