| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2005: ¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 2004: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Research Abstract |
The present investigation aimed to clear the significance and potential participation of oxidized low-density lipoprotein (oxLDL) and neutrophil myeloperoxidase in the pathological mechanism of acute coronary syndrome and other metabolic syndrome-related diseases. The research was performed chiefly by molecular pathological techniques based on the human material. Through this project, we resulted following achievements.
In the first year (May 2004 - March 2005), we reported the localization of oxLDL and the accumulation of neutrophils in culprit lesions of acute coronary syndrome (Am Heart J. 148 : 818-825, 2004) and a close association between platelet activation and neutrophil accumulation in coronary atherosclerotic lesions (Int J Mol Med. 15 : 573-537, 2005). Then, we analyzed oxLDL localization and its receptor expression in human resident macrophages, and revealed that CD36, one of the oxLDL receptors, was induced in the macrophages accumulated in the lesions, suggesting the parti
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cipation of macrophage scavenger receptor in oxLDL clearance (Lung 183 : 109-121, 2005).
In the next year (April 2005 - March 2006), we extended the research objects to find if there were certain relationships between various oxidation factors and pathogenic mechanisms of diverse oxidative stress-related disorders. As a result, we could disclosed that oxLDL played an important role not only in coronary plaque formation and plaque destabilization, but also in continuation of the plaque inflammation after stenting that led to restenosis (Arterioscler Thromb Vasc Biol 26 : 877-883, 2006). OxLDL also played a role in thrombogenesis and calcification in coronary artery lesions (Circulation 112 Suppl.2 : U491, 2005 ; and Circulation 112 Suppl.2 : U585, 2005). Accumulation of oxLDL in affected organs caused from metabolic syndrome was not a limited phenomenon in coronary atherosclerosis. Similar findings were observed in fatty liver disease, and were closely related to marked infiltration of myeloperoxidase-positive neutrophils (Hepatology 43 : 506-514, 2006).
Probably, oxidative stress was a common pathological mechanism in of the development of various metabolic syndrome-related diseases other than coronary artery disease. Because vessels are distributed in every organ/tissue, pathological changes in vessels may affect on a whole body. I would like to continue more extensive investigations about a role for oxidative stress in various metabolic syndrome-related diseases. Less
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