Angiotensin II induces severe aortic aneurysm formation and dissection in CCN2-KO mice
Ang II infusion in CCN2-KO mice dramatically decreased survival evaluated at the 15-day endpoint (Figure 1A ). Some of these mice died as early as at day 2, and post-mortem examination revealed that aortic rupture was the cause of death. Visual aortic evaluation at the endpoint revealed that Ang II-infused CCN2-KO mice significantly developed thoracic and abdominal aorta aneurysms (Thoracoabdominal aneurysms: TAAAs) of all types (according to the Crawford/Safi classification) with a 92 % incidence, while the presence of smaller abdominal aneurysms were found in 30% and 8% of CCN2-KO and WT + Ang II mice, respectively (Figure 1B and C ).
Blood pressure changes were also evaluated. As expected, Ang II administration increased systolic blood pressure in WT mice. However, a similar blood pressure elevation was observed in CCN2-KO mice infused with Ang II for 15 days. On the other hand, in CCN2-KO mice a slight and persistent decrease in systolic blood pressure was observed upon CCN2 deletion (Figure 1D ).