Abstract 15060: Pentraxin 3 Expression in Human Abdominal Aortic Aneurysm
Introduction: Abdominal aortic aneurysm (AAA) is a common degenerative vascular disease among elderly subjects. However, the exact cause of AAA is largely unknown. Pentraxin 3 (PTX3) is an inflammatory protein produced at inflammation sites in response to inflammatory signals, and PTX3 has an anti-inflammatory function in atherosclerotic lesion. Although inflammation plays a critical role in the pathophysiology of AAA, it has not been investigated whether PTX3 is involved in the pathophysiological mechanism of AAA. The aim of this study is to examine PTX3 expression in human AAA tissues.
Methods: Aortic tissue samples were collected from 77 patients undergoing cardiovascular surgery (AAA: n=40, non-AAA: n=37). Non aneurysmal walls were extracted from ascending aortas of patients undergoing aortic valve replacement for aortic valve stenosis or aortic valve regurgitation at the time of establishment of cardiopulmonary bypass. Patients with significant diseases such as autoimmune diseases, infections, cancer, or renal failure were excluded. Serum PTX3 levels were examined by ELISA, and aortic PTX3 expression was determined by Western blot and immunohistochemical analyses.
Results: The proportion of male patients was higher in AAA group than non-AAA group (84 vs 38%, p<0.05), while there was no significant difference in medication between two groups. Serum PTX3 levels were not different between two groups (AAA vs non-AAA; 3.23 vs 2.62 ng/ml). On the other hand, aortic PTX3 expression was markedly increased in AAA tissues compared with non-AAA tissues. Histological analysis revealed that PTX3 was mainly expressed in thickened intima of AAA tissues. Interestingly, the extent of PTX3 positive area was negatively correlated with maximum aortic diameter (r=0.74, p<0.05).
Conclusions: PTX3 expression was markedly increased in AAA tissues. These results suggest that PTX3 is involved in the pathophysiological mechanism of AAA.
Author Disclosures: H. Sawada: None. Y. Naito: None. M. Oboshi: None. T. Iwasaku: None. D. Morisawa: None. Y. Okuhara: None. A. Eguchi: None. S. Hirotani: None. T. Mano: None. T. Masuyama: None.
- © 2014 by American Heart Association, Inc.