title: Angiotensin (1-7) ameliorates angiotensin II-induced inflammation by inhibiting LOX-1 expression.
abstract: OBJECTIVE
  Endothelial dysfunction plays an important role in all stages of atherosclerosis and is characterized by an increased proinflammatory response. This study investigated the effect of angiotensin (1-7) on angiotensin II (Ang II)-mediated inflammation in endothelial cells (ECs) and uncovered its molecular mechanism.
  
  
  RESULTS
  Real-time PCR and western blot analysis were used to determine lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) expression. Ang II treatment induced inflammation, as measured by the production of vascular cell adhesion molecule-1 and monocyte chemoattractant protein-1, by activating nuclear factor-κB (NF-κB) in ECs. Ang II also induced LOX-1 expression in human ECs and rabbit aortic ECs. LOX-1 played an essential role in Ang II-mediated inflammation because Ang II antagonists or small interference RNA significantly decreased Ang II-induced VCAM-1 production. LOX-1 overexpression enhanced Ang II-mediated inflammation. LOX-1 mediated Ang II-induced inflammation by inducing NF-κB DNA-binding activity. Angiotensin (1-7) inhibited LOX-1 expression and diminished Ang II-mediated inflammation in ECs.
  
  
  CONCLUSIONS
  Our findings suggest that angiotensin (1-7) prevents Ang II-induced inflammation by inhibiting LOX-1 mRNA and protein expression in ECs and may represent a novel pleiotropic effect of angiotensin (1-7).
authors.affiliation: Department of Cardiology, Shenzhen Baoan District People's Hospital, Shenzhen 518101, Guangdong, People's Republic of China. wanglj63@163.com
authors.forename: Lijun
authors.initials: L
authors.lastname: Wang
authors.forename: Xuesong
authors.initials: X
authors.lastname: Hu
authors.forename: Wenwu
authors.initials: W
authors.lastname: Zhang
authors.forename: Fang
authors.initials: F
authors.lastname: Tian
mesh_terms: D000803:Angiotensin I / Q000378:metabolism*; D000804:Angiotensin II / Q000378:metabolism*; D000818:Animals; D002448:Cell Adhesion; D018932:Chemokine CCL2 / Q000378:metabolism; D004247:DNA / Q000378:metabolism; D042783:Endothelial Cells / Q000187:drug effects / Q000378:metabolism; D005260:Female; D006801:Humans; D007249:Inflammation / Q000378:metabolism*; D008297:Male; D016328:NF-kappa B / Q000378:metabolism; D010446:Peptide Fragments / Q000378:metabolism*; D011817:Rabbits; D051127:Scavenger Receptors, Class E / Q000037:antagonists & inhibitors* / Q000235:genetics / Q000378:metabolism; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism
chemical_list: D018932:Chemokine CCL2; D016328:NF-kappa B; D010446:Peptide Fragments; D051127:Scavenger Receptors, Class E; D019010:Vascular Cell Adhesion Molecule-1; D000804:Angiotensin II; D004247:DNA; D000803:Angiotensin I; C118790:angiotensin I (1-7)