Left ventricular expression of LOX-1 is markedly increased in proportion to the extent of hypertension-induced heart failure in rats
Tomohide Takaya1, Tatsuya Morimoto1, Yoichi Sunagawa1, Hiromichi Wada1, Teruhisa Kawamura1, Akira Shimatsu1, Masatoshi Fujita3, Yoshiko Fujita2, Tatsuya Sawamura2, Koji Hasegawa1.
- Division of Translational Reseaarch, Kyoto Medical Center, National Hospital Organization, Kyoto, Japan.
- Department Vascular Physiology, National Cardiovascular Center, Osaka, Japan.
- Department of Human Health Sciences, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
第12回日本心不全学会学術集会 (東京), 2008/10/17 (ポスター).
Abstract
Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) was originally identified as an endothelial receptor for oxidized LDL and now recognized as a multi-ligand receptor. LOX-1 expression in cardiomyocytes can be induced by oxidative stress and by various hormonal stimuli. Activation of LOX-1 pathway in cardiomyocytes induces apoptosis of these cells. However the role of LOX-1 in the development of heart failure in vivo is unknown. We examined left ventricular (LV) expression of LOX-1 in salt-sensitive Dahl (DS) rat model of hypertension. Compared with control salt-resistant Dahl rats, high-salt diet resulted in hypertension and apparent concentric LV hypertrophy by echocardiography in DS rats. LV systolic function were preserved at 11 weeks, and decreased at 18 weeks. Quantitative real-time PCR revealed increase in LV levels of LOX-1 mRNA in DS rats compared with DR rats by 4.7-fold at 11 weeks and by 32-fold at 18 weeks. LV LOX-1 mRNA levels were significantly correlated with LV end-systolic dimension (R = 0.640, p = 0.0002) and LV posterior wall thickness (R = 0.555, p = 0.0022). Importantly, LOX-1 levels were strongly correlated with decrease in LV ejection fraction (R = 0.774, p < 0.0001) and increase in mRNA levels of BNP (R = 0.814, p < 0.0001), a representative marker of LV wall stress and heart failure. These findings demonstrate that LV expression of LOX-1 is markedly increased in proportion to the extent of hypertension-induced heart failure.