Figure 1.

Expression and function of TNC in mouse model of aortic diseases. Upper panel: Application of CaCl₂ solution to the lower abdominal aorta caused local inflammation and formation of aortic aneurysm. Continuous infusion of angiotensin II after the CaCl₂ application resulted in higher wall stress and formation of larger aortic aneurysm. TNC was induced in the lower abdominal aorta by CaCl₂-induced local inflammation, and in the thoracic and upper abdominal aorta due to the angiotensin II-induced higher wall stress, as illustrated by the blue color. Lower panel: TNC-deficient mice developed aortic aneurysm comparable to wild-type mice by CaCl₂ application in the presence or absence of angiotensin II. On the other hand, TNC-deficient mice developed aortic dissection in the thoracic and upper abdominal aorta that was characterized by the disruption of the aortic wall (arrowheads) and the formation of false lumen (red color). These findings indicate that TNC does not play a major role in the destructive inflammation in the aortic aneurysm, while it is critical for protecting the aortic wall from dissection, exemplifying the context-dependent function of TNC (111).