Aquaporin 1 does not contribute to the progression of abdominal aortic aneurysm in mice

Abstract

Abdominal aortic aneurysm (AAA) is an asymptomatic chronic dilatation of the abdominal aorta observed predominantly in elderly males. The disease is usually first discovered at the time of rupture and often has a lethal outcome. The mechanism of aneurysm progression is not well characterized, but includes extensive vascular remodeling. Aquaporin 1 (AQP1) is necessary for endothelial‐ and vascular smooth muscle cell migration in tumors and in hypoxic conditions. Thus, we hypothesized that deletion of AQP1 attenuates the formation and progression of abdominal aortic aneurysms. 10–12 weeks old male ApoE KO and AQP1‐ApoE dKO mice were fed western diet and given angiotensin II (Ang II, 1 μg/kg/min) via subcutaneous osmotic mini pumps for 28 days in order to increase blood pressure and induce AAA formation. At 28 days mice were euthanized and aorta dissected. As expected plasma Ang II concentration did not differ between ApoE KO and AQP1‐ApoE dKO mice (403 ± 96 pg/ml vs. 370 ± 74 pg/ml, n=10–11, p=0.8). There was no difference in the incidence of AAA formation (64% vs. 61%). AAA sizes were similar in ApoE KO and AQP1‐ApoE dKO mice, as measured by outer abdominal diameter (1.45 ± 0.18 mm vs. 1.25 ± 0.18 mm, n = 10–11, p=0.4), and by wet weight of the abdominal aorta (15.4 ± 3.7 mg vs. 14.7 ± 4.3 mg, n= 10–11, p=0.9). It is concluded that in ApoE KO mice on western diet, AQP1 does not contribute significantly to incidence and progression of abdominal aorta aneurysm.Supported by Alfred Andersen grant and Director Jacob Madsen & Olga Madsen's grant