徳島大学 教育・研究者情報データベース(EDB)

1. (英) Tsujita Kenichi

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2. (英) Kaikita Koichi

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3. (英) Hayasaki Takanori

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4. (英) Honda Tsuyoshi

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5. (英) Kobayashi Hironori

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6. 坂下 直実

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7. (英) Suzuki Hiroshi

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8. (英) Kodama Tatsuhiko

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9. (英) Ogawa Hisao

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10. (英) Takeya Motohiro

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(英) Targeted deletion of class A macrophage scavenger receptor increases the risk of cardiac rupture after experimental myocardial infarction.

(英) Class A macrophage scavenger receptor (SR-A) is a macrophage-restricted multifunctional molecule that optimizes the inflammatory response by modulation of the activity of inflammatory cytokines. This study was conducted with SR-A-deficient (SR-A(-/-)) mice to evaluate the relationship between SR-A and cardiac remodeling after myocardial infarction. Experimental myocardial infarction (MI) was produced by ligation of the left coronary artery in SR-A(-/-) and wild-type (WT) male mice. The number of mice that died within 4 weeks after MI was significantly greater in SR-A(-/-) mice than in WT mice (P=0.03). Importantly, death caused by cardiac rupture within 1 week after MI was 31% (17 of 54 mice) in SR-A(-/-) mice and 12% (6 of 51 mice) in WT mice (P=0.01). In situ zymography demonstrated augmented gelatinolytic activity in the infarcted myocardium in SR-A(-/-) mice compared with WT mice. Real-time reverse transcription-polymerase chain reaction at day 3 after MI showed that the expression of matrix metalloproteinase-9 mRNA increased significantly in the infarcted myocardium in SR-A(-/-) mice compared with WT mice. Furthermore, SR-A(-/-) mice showed augmented expression of tumor necrosis factor-alpha and reduction of interleukin-10 in the infarcted myocardium at day 3 after MI. In vitro experiments also demonstrated increased tumor necrosis factor-alpha and decreased interleukin-10 expression in activated SR-A(-/-) macrophages. The present findings suggest that SR-A deficiency might cause impairment of infarct remodeling that results in cardiac rupture via insufficient production of interleukin-10 and enhanced expression of tumor necrosis factor-alpha and of matrix metalloproteinase-9. SR-A might contribute to the prevention of cardiac rupture after MI.

1. (英) Animals
2. (英) Cells, Cultured
3. (英) Crosses, Genetic
4. 細胞質分裂(cytokinesis)
5. (英) Enzyme Induction
6. (英) Gene Deletion
7. (英) Heart Rupture
8. (英) Interleukin-10
9. (英) Lipoproteins, LDL
10. (英) Macrophages, Peritoneal
11. 男性(male)
12. (英) Matrix Metalloproteinase 2
13. (英) Matrix Metalloproteinase 9
14. (英) Mice
15. (英) Mice, Inbred C57BL
16. ノックアウトマウス(knockout mice)
17. (英) Myocardial Infarction
18. 心筋(myocardium)
19. (英) Reverse Transcriptase Polymerase Chain Reaction
20. (英) Scavenger Receptors, Class A
21. (英) Tissue Inhibitor of Metalloproteinase-1
22. (英) Tissue Inhibitor of Metalloproteinases
23. (英) Tumor Necrosis Factor-alpha
24. (英) Ventricular Remodeling

1. (英) Article.Affiliation: Department of Cell Pathology, Graduate School of Medical Sciences, Kumamoto University, 1-1-1 Honjo, Kumamoto 860-8556, Japan.

2. (英) Article.PublicationTypeList.PublicationType: Journal Article

3. (英) Article.PublicationTypeList.PublicationType: Research Support, Non-U.S. Gov't