The water channel AQP 1 is expressed in human atherosclerotic vascular lesions and AQP 1 deficiency augments angiotensin II ‐induced atherosclerosis in mice

Aim The water channel aquaporin 1 ( AQP 1) promotes endothelial cell migration. It was hypothesized that AQP 1 promotes neovascularization and growth of atherosclerotic plaques. Methods AQP 1 immunoreactivity and protein abundance was examined in human and murine atherosclerotic lesions and aortic aneurysms. Apolipoprotein E (ApoE) knockout (−/−) and AQP 1−/−ApoE−/− mice were developed and fed Western diet ( WD ) for 8 and 16 weeks to accelerate the atherosclerosis process. In ApoE−/− and AQP 1−/−ApoE−/− mice abdominal aortic aneurysms ( AAA ) were induced by angiotensin II ( ANGII ) infusion by osmotic minipumps for 4 weeks. Results In human atherosclerotic lesions and AAA, AQP1 immunoreactive protein was associated with intralesional small vessels. In ApoE−/− mouse aorta, APQ 1 mRNA levels were increased with time on WD ( n  = 7–9, P  < 0.003). Both in murine lesions at the aortic root and in the abdominal aortic aneurysmal wall, AQP 1 immunoreactivity was associated with microvascular structures. The atherosclerotic lesion burden was enhanced significantly in ANGII ‐infused AQP 1−/−ApoE−/− mice compared with ApoE−/− mice, but neither incidence nor progression of AAA was different. The aortic lesion burden increased with time on WD but was not different between ApoE−/− and AQP 1−/−ApoE−/− mice at either 8 or 16 weeks ( n  = 13–15). Baseline blood pressure and ANGII ‐induced hypertension were not different between genotypes. Conclusion AQP 1 is expressed in atherosclerotic lesion neovasculature in human and mouse arteries and AQP 1 deficiency augments lesion development in ANGII ‐promoted atherosclerosis in mice. Normal function of AQP 1 affords cardiovascular protection.