title: Left ventricular expression of lectin-like oxidized low-density lipoprotein receptor-1 in failing rat hearts.
abstract: BACKGROUND
  Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) is a multiple ligand receptor induced by oxidative stress. However, its role in chronic heart failure remains unknown.
  
  
  RESULTS
  The left ventricular (LV) expression of LOX-1 was examined in a salt-sensitive Dahl rat model of hypertension. Compared with controls, LOX-1 mRNA levels increased by 4.7-fold in the LV with hypertrophy, and by 32-fold in the LV with decreased systolic function. LV LOX-1 mRNA levels strongly correlated with the decrease in LV ejection fraction (EF) (r=-0.772), and with increases in the LV mRNA levels of B-type natriuretic peptide (r=0.814), monocyte chemoattractant protein-1 (r=0.943), transforming growth factor-beta(1) (r=0.936), and a macrophage marker, F4/80 (r=0.560). Serum levels of soluble LOX-1 were significantly elevated in patients with LV systolic dysfunction and hypertrophy, and significantly correlated with the decrease in EF (r=-0.495).
  
  
  CONCLUSIONS
  Marked increase in the LV expression of LOX-1 in failing hearts may contribute to increased serum levels, and might be involved in chronic inflammation during the development of heart failure.
authors.affiliation: Division of Translational Research, Kyoto Medical Center, National Hospital Organization, Kyoto, Japan.
authors.forename: Tomohide
authors.initials: T
authors.lastname: Takaya
authors.forename: Hiromichi
authors.initials: H
authors.lastname: Wada
authors.forename: Tatsuya
authors.initials: T
authors.lastname: Morimoto
authors.forename: Yoichi
authors.initials: Y
authors.lastname: Sunagawa
authors.forename: Teruhisa
authors.initials: T
authors.lastname: Kawamura
authors.forename: Rieko
authors.initials: R
authors.lastname: Takanabe-Mori
authors.forename: Akira
authors.initials: A
authors.lastname: Shimatsu
authors.forename: Yoshiko
authors.initials: Y
authors.lastname: Fujita
authors.forename: Yuko
authors.initials: Y
authors.lastname: Sato
authors.forename: Masatoshi
authors.initials: M
authors.lastname: Fujita
authors.forename: Takeshi
authors.initials: T
authors.lastname: Kimura
authors.forename: Tatsuya
authors.initials: T
authors.lastname: Sawamura
authors.forename: Koji
authors.initials: K
authors.lastname: Hasegawa
mesh_terms: D000368:Aged; D000818:Animals; D018932:Chemokine CCL2 / Q000097:blood; D003430:Cross-Sectional Studies; D004195:Disease Models, Animal; D005260:Female; D006333:Heart Failure / Q000378:metabolism*; D006352:Heart Ventricles / Q000378:metabolism*; D006801:Humans; D006973:Hypertension / Q000378:metabolism*; D017379:Hypertrophy, Left Ventricular / Q000097:blood; D008297:Male; D008875:Middle Aged; D020097:Natriuretic Peptide, Brain / Q000097:blood; D018384:Oxidative Stress / Q000502:physiology; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D020303:Rats, Inbred Dahl; D051127:Scavenger Receptors, Class E / Q000378:metabolism*; D018487:Ventricular Dysfunction, Left / Q000097:blood
chemical_list: C491766:Ccl2 protein, rat; D018932:Chemokine CCL2; C495136:OLR1 protein, rat; D012333:RNA, Messenger; D051127:Scavenger Receptors, Class E; D020097:Natriuretic Peptide, Brain