Abstract
Treatment with an inhibitor of glucose use via glucose transporters (GLUT) has been shown to attenuate experimental abdominal aortic aneurysm (AAA) development in mice. Vascular smooth muscle cell (VSMC) signaling seems to be essential for angiotensin II (Ang II)-induced AAA in mice. Accordingly, we have tested a hypothesis that VSMC silencing of the major GLUT, GLUT1, prevents AAA development and rupture in mice treated with Ang II plus β-aminopropionitrile. A mouse model of inducible VSMC GLUT1 deletion was created and aortic GLUT1 silencing was confirmed. Without Ang II plus β-aminopropionitrile treatment, no difference was observed regarding the external aortic diameter (control 1.06 ± 0.18 mm vs deletion 0.97 ± 0.26 mm) or systolic blood pressure (control 102 ± 9 mm Hg vs deletion 107 ± 11 mm Hg) between control or GLUT1-silenced mice. With treatment, control mice as well as VSMC GLUT1-silenced mice equally developed AAA (control 2.37 ± 0.75 mm vs deletion 2.41 ± 0.93 mm), whereas a tendency toward lower blood pressure was observed in GLUT1 silenced mice (control 150 ± 9 mm Hg vs deletion 135 ± 22 mm Hg). No significant difference was observed regarding the rate of rupture-dependent mortality. We concluded that VSMC GLUT1 is dispensable for AAA development induced by Ang II in mice.