アクティブボード・２０１０年９月
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研究発表を行った学会；
・第74回日本循環器学会総会・学術総会.
　２０１０年　３月　５日〜７日（京都）

タイトル；Angiopoietin-like protein2 (Angptl2) contributes to the development of aortic aneurysms through increasing the chronic inflammation in aortic walls.
　
発表者；　田爪　宏和　氏
　　　（熊本大学　大学院生命科学研究部　心臓血管外科および分子遺伝学分野）

Abstract；
Abdominal aortic aneurysm (AAA) is characterized by atherosclerotic changes with chronic inflammation of aortic walls. However, the molecular mechanism underlying chronic inflammation in the development of AAA has not been elucidated well. We recently reported that adipocyte-derived Angptl2 is a key mediator linking obesity to adipose tissue inflammation and systemic insulin resistance (Cell Metabolism 2009). Since Angptl2 is expressed in vascular smooth muscle cells as well as adipocytes, we investigated whether Angptl2 is involved in AAA formation. Firstly we found that Angptl2 was expressed in macrophages and vascular smooth muscle cells in outer media and the adventitia at aneurysm site. Therefore, we examined the Angptl2 expression in the process of AAA formation using a CaCl2-induced mouse AAA model. RT-PCR analysis revealed that Angptl2 expression was markedly increased at day 7 after operation and sustained until day 42, while the expression levels of TNFa, IL-6, and IL-1b were peaked at day 3 and decreased rapidly until day 7. We next investigated whether Angptl2 contribute to AAA formation by analyzing Angptl2 KO mice. Interestingly, the size of AAA at day 28 of Angptl2-/- mice was significantly decreased than wild-type mice (n=8, p<0.03). Thus, Angptl2 may be an important mediator causing vascular chronic inflammation in the pathogenesis of aortic aneurysm. The present findings would also lead to new treatment strategies for aortic aneurysm.