2008

DOI: 10.1136/hrt.2007.121640

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Increased serum levels and expression of S100A8/A9 complex in infiltrated neutrophils in atherosclerotic plaque of unstable angina

Shoichi Miyamoto

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et al.

Abstract: The S100A8/A9 complex may be involved in the inflammatory process of coronary atherosclerotic plaques in patients with UA.

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Ionita Et Al Mrp-14 In Atherosclerotic Plaque 12231

Editorial P 6261

Produtos De Glicação Avançada E Inflamação1

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Cited by 59 publications

(58 citation statements)

References 26 publications

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“…18 In acute coronary syndrome, S100A8/S100A9 was found to be markedly expressed at the site of coronary occlusion by invading phagocytes. 19 In the present study, we extend these findings by showing increased expression of S100A8/S100A9 within carotid plaques from those patients with the most recent symptoms. Although there are several studies that Figure 1.…”

Section: Discussionsupporting

confidence: 70%

High Levels of S100A12 Are Associated With Recent Plaque Symptomatology in Patients With Carotid Atherosclerosis

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et al. 2012

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Background and Purpose-Atherosclerosis is a progressive chronic disease, in which inflammation plays a key role. The calcium-binding proteins calgranulins including S100A8, S100A9, and S100A12 are involved in many cellular activities and pathological processes including inflammation. We therefore hypothesized that calgranulins may be markers of plaque instability in patients with carotid atherosclerosis. Methods-Plasma levels of S100A8/A9 and S100A10 were measured in 159 consecutive patients with high-grade carotid stenosis and in 22 healthy control subjects. The mRNA levels of calgranulins were also measured within the atherosclerotic carotid plaques, and their regulation was analyzed in vitro in monocytes. Results-Our main findings were: (1) plasma levels of S100A12 were significantly higher in patients with carotid atherosclerosis compared with healthy control subjects with the highest levels in patients with the most recent symptoms (ie, within 2 months); (2) plasma levels of S100A8/S100A9 showed a modest increase in patients with symptoms in the previous 2 to 6 months but not in the other patients; (3) mRNA levels of S100A8, S100A9, and S100A12 showed increased expression in atherosclerotic carotid plaques from patients with the most recent symptoms compared with the remaining patients; (4) in THP-1 monocytes, activation of Toll-like receptors 2 and 4 increased mRNA levels of S100A8, S100A9, and S10012 and interleukin-1␤, interferon ␥, and releasate from thrombin-activated platelets significantly enhanced the expression of S100A12. Conclusions-Our findings support a link between calgranulins and atherogenesis and suggest that these mediators, and in particular S100A12, may be related to plaque instability. (Stroke. 2012;43:1347-1353.)

“…18 In acute coronary syndrome, S100A8/S100A9 was found to be markedly expressed at the site of coronary occlusion by invading phagocytes. 19 In the present study, we extend these findings by showing increased expression of S100A8/S100A9 within carotid plaques from those patients with the most recent symptoms. Although there are several studies that Figure 1.…”

Section: Discussionsupporting

confidence: 70%

High Levels of S100A12 Are Associated With Recent Plaque Symptomatology in Patients With Carotid Atherosclerosis

¹

,

et al. 2012

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Background and Purpose-Atherosclerosis is a progressive chronic disease, in which inflammation plays a key role. The calcium-binding proteins calgranulins including S100A8, S100A9, and S100A12 are involved in many cellular activities and pathological processes including inflammation. We therefore hypothesized that calgranulins may be markers of plaque instability in patients with carotid atherosclerosis. Methods-Plasma levels of S100A8/A9 and S100A10 were measured in 159 consecutive patients with high-grade carotid stenosis and in 22 healthy control subjects. The mRNA levels of calgranulins were also measured within the atherosclerotic carotid plaques, and their regulation was analyzed in vitro in monocytes. Results-Our main findings were: (1) plasma levels of S100A12 were significantly higher in patients with carotid atherosclerosis compared with healthy control subjects with the highest levels in patients with the most recent symptoms (ie, within 2 months); (2) plasma levels of S100A8/S100A9 showed a modest increase in patients with symptoms in the previous 2 to 6 months but not in the other patients; (3) mRNA levels of S100A8, S100A9, and S100A12 showed increased expression in atherosclerotic carotid plaques from patients with the most recent symptoms compared with the remaining patients; (4) in THP-1 monocytes, activation of Toll-like receptors 2 and 4 increased mRNA levels of S100A8, S100A9, and S10012 and interleukin-1␤, interferon ␥, and releasate from thrombin-activated platelets significantly enhanced the expression of S100A12. Conclusions-Our findings support a link between calgranulins and atherogenesis and suggest that these mediators, and in particular S100A12, may be related to plaque instability. (Stroke. 2012;43:1347-1353.)

“…This observation coupled with the positive correlation between IL-8 and Mrp-8, -14, -8/14 plaque levels might suggest a possible role for neutrophils in plaque associated inflammation. A recent study 34 demonstrated that the infiltrated neutrophils within atherectomy specimens of patients with unstable angina were Mrp-8/14 -positive. Although the focus of the present study was on the Mrp-subset of nonfoam plaque macrophages, it does not exclude the importance of other possible Mrp-cellular sources within plaque (eg, the neutrophils).…”

Section: Ionita Et Al Mrp-14 In Atherosclerotic Plaque 1223mentioning

confidence: 99%

High Levels of Myeloid-Related Protein 14 in Human Atherosclerotic Plaques Correlate With the Characteristics of Rupture-Prone Lesions

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et al. 2009

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Objective-Atherosclerotic plaque rupture can lead to severe complications such as myocardial infarction and stroke.Myeloid related protein (Mrp)-14, Mrp-8, and Mrp-8/14 complex are inflammatory markers associated with myocardial infarction. It is, however, unknown whether Mrps are associated with a rupture-prone plaque phenotype. In this study, we determined the association between Mrp-14, -8, -8/14 plaque levels and plaque characteristics. Methods and Results-In 186 human carotid plaques, levels of Mrp-14, -8, and -8/14 were quantified using ELISA. High levels of Mrp-14 were found in lesions with a large lipid core, high macrophage staining, and low smooth muscle cell and collagen amount. Plaques with high levels of Mrp-14 contained high interleukin (IL)-6, IL-8, matrix metalloprotease (MMP)-8, MMP-9, and low MMP-2 concentrations. Mrp-8 and Mrp-8/14 showed a similar trend. Within plaques, a subset of nonfoam macrophages expressed Mrp-8 and Mrp-14 and the percentage of Mrp-positive macrophages was higher in rupture-prone lesions compared to stable ones. In vitro, this subset of macrophages does not acquire a foamy phenotype when fed oxLDL. Conclusion-Mrp-14 is strongly associated with the histopathologic features and the inflammatory status of rupture-prone atherosclerotic lesions, identifying Mrp-14 as a local marker for these plaques.

“…Recent clinical studies have demonstrated elevated serum levels of the S100A8/A9 complex in inflammatory disorders, such as rheumatoid arthritis, 3 transplant rejection, 4 unstable angina pectoris (UAP), 5 acute myocardial infarction (AMI), 6,7 and recent MI. 8 Overexpression of the S100A8/A9 complex has been shown immunohistochemically in atherosclerotic plaques in coronary and carotid arteries.…”

Section: Editorial P 626mentioning

confidence: 99%

Enhanced Expression of the S100A8/A9 Complex in Acute Myocardial Infarction Patients

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et al. 2010

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Background: S100A8/A9 complex (S100A8/A9) is expressed in activated human neutrophils and macrophages. Enhanced expression of S100A8/A9 in atherosclerotic plaque of patients with unstable angina pectoris (UAP) has been demonstrated, but its profile in acute myocardial infarction (AMI) has not been clarified. Methods and Results:Serum S100A8/A9 levels were serially measured in patients with AMI (n=55) and UAP (n=16) during the acute period. The expression of S100A8/A9 was examined immunohistochemically in the infarcted myocardium of 7 autopsied patients with AMI. Serum S100A8/A9 levels on the 1st day were 1,118±115 (SE) ng/ml in AMI patients as compared with 787±147 ng/ml in UAP patients. On days 3-5, serum S100A8/A9 levels in AMI patients reached a peak value and were significantly higher than the values in UAP patients (1,690±144 ng/ml vs 844±100 ng/ml; P<0.0001). In AMI patients, peak S100A8/A9 levels positively correlated with peak white blood cell and neutrophil counts, and peak creatine kinase-MB and peak C-reactive protein levels. Double immunostaining revealed that S100A8/A9 was specifically expressed in neutrophils and macrophages infiltrating the infarcted myocardium.Conclusions: S100A8/A9 is implicated in the pathophysiology of AMI and may be an additional biomarker of the local inflammatory response following AMI. (Circ J 2010; 74: 741 - 748)

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