Toll-like receptor 4 expressions on peripheral blood monocytes were enhanced in coronary artery disease even in patients with low C-reactive protein

Life Sciences ◽  
2006 ◽  
Vol 80 (1) ◽  
pp. 59-66 ◽  
Author(s):  
Rio Shiraki ◽  
Nobutaka Inoue ◽  
Seiichi Kobayashi ◽  
Junya Ejiri ◽  
Kazunori Otsui ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Peripheral Blood ◽  
Toll Like Receptor ◽  
Blood Monocytes ◽  
C Reactive Protein ◽  
Toll Like Receptor 4 ◽  
Peripheral Blood Monocytes ◽  
Reactive Protein ◽  
Artery Disease

Expression of miR-146a/b is associated with the Toll-like receptor 4 signal in coronary artery disease: effect of renin–angiotensin system blockade and statins on miRNA-146a/b and Toll-like receptor 4 levels

2010 ◽  
Vol 119 (9) ◽  
pp. 395-405 ◽  
Author(s):  
Yuji Takahashi ◽  
Mamoru Satoh ◽  
Yoshitaka Minami ◽  
Tsuyoshi Tabuchi ◽  
Tomonori Itoh ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Peripheral Blood ◽  
Combined Treatment ◽  
Renin Angiotensin System ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Angiotensin System ◽  
Tlr4 Mrna ◽  
Artery Disease

The TLR4 (Toll-like receptor 4) signal plays an important role in immunity in CAD (coronary artery disease). miR-146a/b (where miR is microRNA) regulates the TLR4 downstream molecules IRAK1 (interleukin-1-receptor-associated kinase 1) and TRAF6 (tumour-necrosis-factor-receptor-associated factor 6). It has also been reported that statins and RAS (renin–angiotensin system) inhibition and have anti-atherosclerotic properties. In the present study, we have investigated whether miR-146a/b was expressed with the TLR4 signal in CAD patients, and whether combined treatment with a statin and RAS inhibition might affect these levels. A total of 66 patients with CAD and 33 subjects without CAD (non-CAD) were enrolled. Patients with CAD were randomized to 12 months of combined treatment with atorvastatin and telmisartan [an ARB (angiotensin II receptor blocker)] or atorvastatin and enalapril [an ACEI (angiotensin-converting enzyme inhibitor)]. PBMCs (peripheral blood mononuclear cells) were obtained from peripheral blood at baseline and after 12 months. Levels of miR-146a/b, IRAK1 mRNA, TRAF6 mRNA and TLR4 mRNA/TLR4 protein were significantly higher in the CAD group than in the non-CAD group (all P<0.01). Levels of miR-146a/b were positively correlated with IRAK1 mRNA and TRAF6 mRNA levels. After 12 months of treatment, these levels were markedly decreased in the ARB and ACEI groups, with the decrease in the ARB group being greater than that in the ACEI group (all P<0.05). In our 12-month follow-up study, high levels of miR-146a and TLR4 mRNA/TLR4 protein at baseline were independent predictors of cardiac events. The present study demonstrates that combined treatment with an ARB and a statin decreases miR-146a/b and the TLR4 signal in CAD patients, possibly contributing to the anti-atherogenic effects of ARBs and statins in this disorder.

scholarly journals The p66shc Gene Expression in Peripheral Blood Monocytes Is Increased in Patients With Coronary Artery Disease

2010 ◽  
Vol 33 (9) ◽  
pp. 548-552 ◽  
Author(s):  
Yoshihiro Noda ◽  
Sho-ichi Yamagishi ◽  
Takanori Matsui ◽  
So Ueda ◽  
Shin-ichiro Ueda ◽  
...  
Keyword(s):  
Gene Expression ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Peripheral Blood ◽  
Blood Monocytes ◽  
Peripheral Blood Monocytes ◽  
Artery Disease

Common polymorphisms of cyclooxygenase-2 and prostaglandin E2 receptor and increased risk for acute coronary syndrome in coronary artery disease

2008 ◽  
Vol 100 (05) ◽  
pp. 893-898 ◽  
Author(s):  
Wojciech Szczeklik ◽  
Marek Sanak ◽  
Pawel Rostoff ◽  
Wieslawa Piwowarska ◽  
Bogdan Jakiela ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Peripheral Blood ◽  
Pge2 Production ◽  
Blood Monocytes ◽  
Wild Type ◽  
Peripheral Blood Monocytes ◽  
Cox 2 ◽  
Artery Disease ◽  
Ep2 Receptor

SummaryThe arachidonic acid metabolites participate in development of coronary artery disease (CAD) and the plaque’s instability.We assessed two common genetic polymorphisms: of cyclooxyge-nase-2 (COX-2) (COX 2.8473, rs5275) and prostaglandin EP2 receptor gene (uS5, rs708494) in patients with CAD. Out of 1,368 patients screened by coronary arteriography, two groups fulfilled the entry criteria and were studied: stable coronary disease (sCAD, n=125) and acute coronary syndromes (ACS, n=63).They did not differ in the main characteristics.All patients were on aspirin at least seven days prior to the study.In 70 control subjects, the same genotypes were ascertained, expression of cyclooxygenases in peripheral blood monocytes was assessed by flow cytometry, and in-vitro biosynthesis of PGE2 was measured by mass spectrometry. COX-2 CC homozygotes (variant allele), were more common, while EP2 GG homozygotes (wild-type) were less common in ACS (p=0.03 and p=0.017) than in the sCAD group.A combined genotype characterized by the presence of the wild-type COX2.8743T allele and the wild type homozygous EP2uS5 genotype (TT or CT | GG) decreased risk ratio of ACS in CAD patients (relative risk 0.41;95% confidence interval 0.21–0.81).COX-2 polymorphism in control subjects did not affect the enzyme expression or PGE2 production by peripheral blood monocytes, but production of PGE2 increased by 40.1% in the subjects homozygous for EP2 receptor allele uS5A following lipopolysaccharide stimulation. In conclusion, the combined COX-2 (COX 2.8473) and the EP2 receptor (uS5) genotypes seem to influence CAD stability, but in peripheral blood monocytes only EP2 receptor modulates PGE2 production.

Pentraxin-3 as a more sensitive marker of coronary artery disease severity than C-reactive protein

2013 ◽  
Author(s):  
Janusz Szkodzinski ◽  
Bartosz Hudzik ◽  
Aleksander Danikiewicz ◽  
Anna Pietka-Rzycka ◽  
Andrzej Lekston ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Disease Severity ◽  
Pentraxin 3 ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Coronary Artery Disease Severity ◽  
Artery Disease ◽  
Sensitive Marker
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