1. Chemokine (C–X–C motif) receptor 2 blockade by SB265610 inhibited angiotensin II-induced abdominal aortic aneurysm in Apo E−/− mice
- Author
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Hui-Hua Li, Fang-Da Li, Hua-liang Ren, Chao-Yu Wang, Yuehong Zheng, Hao Nie, Hong-Xia Wang, and Cui Tian
- Subjects
Male ,Apolipoprotein E ,Chemokine ,Mice, Knockout, ApoE ,Inflammation ,macromolecular substances ,030204 cardiovascular system & hematology ,Pharmacology ,Receptors, Interleukin-8B ,Mice ,03 medical and health sciences ,Chemokine receptor ,0302 clinical medicine ,medicine ,Animals ,Humans ,cardiovascular diseases ,030212 general & internal medicine ,CXC chemokine receptors ,Receptor ,biology ,business.industry ,Angiotensin II ,Macrophages ,Phenylurea Compounds ,hemic and immune systems ,Chemotaxis ,Triazoles ,respiratory tract diseases ,Disease Models, Animal ,cardiovascular system ,biology.protein ,medicine.symptom ,Cardiology and Cardiovascular Medicine ,business ,Aortic Aneurysm, Abdominal ,Signal Transduction - Abstract
Inflammation plays a critical role in the development of abdominal aortic aneurysm (AAA). Chemokine receptor CXCR2 mediates inflammatory cell chemotaxis in several diseases. However, the role of CXCR2 in AAA and the underlying mechanisms remain unknown. In this study, we found that the CXCR2 expressions in AAA tissues from human and angiotensin II (Ang II)-infused apolipoprotein E knockout (Apo E-/-) mice were significantly increased. The pharmacological inhibition of CXCR2 (SB265610) markedly reduced Ang II-induced AAA formation. Furthermore, SB265610 treatment significantly reduced collagen deposition, elastin degradation, the metal matrix metalloprotease expression and accumulation of macrophage cells. In conclusion, these results showed CXCR2 plays a pathogenic role in AAA formation. Inhibition of CXCR2 pathway may represent a novel therapeutic approach to treat AAA.
- Published
- 2018