Enhanced Expression of the S100A8/A9 Complex in Acute Myocardial Infarction Patients
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- Katashima Takashi
- Department of Internal Medicine III, Osaka Medical College
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- Naruko Takahiko
- Department of Cardiology, Osaka City General Hospital
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- Terasaki Fumio
- Department of Internal Medicine III, Osaka Medical College
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- Fujita Masatoshi
- Human Health Sciences, Kyoto University Graduate School of Medicine
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- Otsuka Kaoru
- Department of Internal Medicine III, Osaka Medical College
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- Murakami Shougo
- Department of Internal Medicine III, Osaka Medical College
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- Sato Akira
- Department of Cardiology, University of Tsukuba Graduate School of Comprehensive Human Science
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- Hiroe Michiaki
- Department of Cardiology, International Medical Center of Japan
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- Ikura Yoshihiro
- Department of Pathology, Osaka City University Graduate School of Medicine
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- Ueda Makiko
- Department of Pathology, Osaka City University Graduate School of Medicine
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- Ikemoto Masaki
- Human Health Sciences, Kyoto University Graduate School of Medicine
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- Kitaura Yasushi
- Department of Internal Medicine III, Osaka Medical College
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Abstract
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)<br>
Journal
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- Circulation Journal
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Circulation Journal 74 (4), 741-748, 2010
The Japanese Circulation Society
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Details 詳細情報について
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- CRID
- 1390001205101897984
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- NII Article ID
- 10026472579
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- NII Book ID
- AA11591968
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- ISSN
- 13474820
- 13469843
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- Text Lang
- en
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- Data Source
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- JaLC
- Crossref
- CiNii Articles
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- Abstract License Flag
- Disallowed