522 高血圧下の初期動脈硬化形成のメカニズム : 酸化LDL受容体LOX-1の意義(T10-1 マイクロ・ナノバイオテクノロジー(1):細胞の応答とその応用,大会テーマセッション,21世紀地球環境革命の機械工学:人・マイクロナノ・エネルギー・環境)

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Hypertension is a powerful independent risk factor for atherosclerotic cardiovascular diseases; however, the precise molecular mechanisms whereby hypertension promotes atherosclerotic formation remain to be determined. The interaction of oxidized low density lipoprotein (LDL) and lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) plays a critical role in atherogenesis. To investigate their specific roles in acceleration of atherogenesis by hypertension, here, we employed stroke prone spontaneously hypertensive rats (SHR-SP), models of human essential hypertension, rapidly developed arterial lipid deposition in mesenteric arteries when fed on high fat diet and salt loading. These vascular lipid deposition lesions share similar characteristics of the initial lesions of atherosclerosis. The enhanced LOX-1 expression in SHR-SP was closely associated with deposited lipids, oxidized LDL, and generation of reactive oxygen species. Anti-LOX-1 neutralizing antibody dramatically suppressed lipid deposition in vivo in SHR-SP. Vitamin E decreased plasma oxidized LDL, which suppressed the lipid deposition as well. Furthermore, anti-LOX-1 antibody suppressed the increase in vascular permeability and uptake of oxidized LDL in SHR-SP. Thus, the enhanced expression and activation of LOX-1 leading to an increase in vascular permeability and oxidative stress plays an essential role in vascular lipid deposition under hypertensive states.
社団法人日本機械学会の論文
2008-08-02

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