Abstract
Objective: Chronic infusion of angiotensin II (AngII) promotes development of abdominal aortic aneurysms (AAAs) in Apolipoprotein E-deficient (ApoE-/-) mice. Interleukin 33 (IL-33), known as one of IL-1 family, is rapidly released from damaged endothelial and epithelial cells. IL-33 binds to its receptor, ST2, and exerts various physiological functions through its downstream signaling. Previous studies have shown that exogenous IL-33 attenuates development of AAAs through wound healing resolution. The purpose of this study was to evaluate whether IL-33 deficiency exacerbated development of AAAs by using IL-33xApoE double deficient (IL-33-/-xApoE-/-) mice. Methods and Results: Male ApoE-/- and IL-33-/-xApoE-/- (8-12 weeks old) mice were assigned into saline infused group (ApoE-/- n=5, IL-33-/-xApoE-/- n=7) and AngII infused group (ApoE-/- n=19, IL-33-/-xApoE-/- n=19). Mice were infused subcutaneously with either saline or AngII by osmotic minipumps for 4 weeks. During 4-week AngII infusion, 3 mice died by AAA rupture in each AngII-infused group. There was no significant difference in ex vivo abdominal aortic width between saline infused groups (ApoE-/- 0.87±0.17 mm vs IL-33-/-xApoE-/- 0.87±0.14 mm, n.s.) nor body weight (ApoE-/- 27.3±0.9 g vs IL-33-/-xApoE-/- 27.9±0.9 g, n.s.) but serum total cholesterol concentrations in IL-33-/-xApoE-/- was higher than in ApoE-/- (522±85 mg/dL vs 427±108 mg/dL, p=0.026). AngII equally elevated systolic blood pressure (ApoE-/- 151±15 mmHg, IL-33-/-xApoE-/- 155±17 mmHg, n.s.). AngII increased ex vivo maximum abdominal aortic width in AngII infused groups, but AAAs were further exacerbated in the group of IL-33-/-xApoE-/- mice (ApoE-/- 1.31±0.09 mm vs IL-33-/-xApoE-/- 1.76±0.09 mm, p=0.001). In addition, the severity of AAAs in AngII infused groups was significantly worse in IL-33-/-xApoE-/- than in ApoE-/- (p=0.037). Conclusion: Our study demonstrated IL-33 deficiency exacerbated AngII-induced AAAs in male ApoE-/- mice.
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