Angiotensin (1-7) ameliorates angiotensin II-induced inflammation by inhibiting LOX-1 expression

作者：Wang Lijun^*; Hu Xuesong; Zhang Wenwu; Tian Fang

来源：Inflammation Research, 2013, 62(2): 219-228.

DOI：10.1007/s00011-012-0571-2

• Ang (1-7)
• Ang II
• LOX-1
• Endothelial cells
• Inflammation

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.
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-kappa B (NF-kappa B) 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-kappa B DNA-binding activity. Angiotensin (1-7) inhibited LOX-1 expression and diminished Ang II-mediated inflammation in ECs.
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).

• 出版日期2013-2