Abstract 18391: Accumulation of Adiponectin in Association With Up-regulated T-cadherin in the Aortic Wall of Acute and Chronic Aortic Dissection
Introduction: Adiponectin (APN) is a major adipokine, which has been reported to accumulate into the damaged tissues in multiple organs. However, the role of APN and its receptor, T-cadherin (T-cad), in the pathology of the human aortic wall (AW) is poorly understood. In this study, we examined the distributions of APN and T-cad in the dissected AW and measured the serum APN concentration in patients with aortic dissection (AD).
Methods: Diseased AW tissues were collected from patients with acute or chronic AD at the time of surgery, and a healthy aorta was used as a control (n = 6 per group). Blood was serially sampled to measure the APN concentrations in non-surgically-treated patients with acute type B AD (n = 10).
Results: Immunohistochemically, normal aortic walls weakly expressed APN or T-cad on the intimal surface, whereas the AWs of acute AD patients showed marked expression of both APN and T-cad on the surface of the dissected aortic media. In chronic AD, APN and T-cad were diffusely expressed on the medial layers of the thickened AW (Fig. A-C). Western blot analysis showed that APN expression in the AW was significantly greater in acute and chronic AD than in the normal aorta (151 ± 2% and 220 ± 27% vs. normal, respectively) (Fig. D). RT-PCR revealed no expression of APN mRNA in any AW, and stronger expression of T-cad mRNA in acute and chronic AD than in the normal aorta (108 ± 9% and 194 ± 101% vs. normal, respectively). The blood concentration of APN in type B AD patients decreased by 13.3 ± 3.8% in 24-78 hours, and by 22.7 ± 7.2% in over 78 hours, as compared to those monitored within 24 hours after the onset, indicating that APN was supplied to the affected aortic wall from the blood.
Conclusions: APN markedly accumulated into the dissected aortic media in acute and chronic AD, and T-cad was upregulated in the corresponding area. In contrast, the blood concentration of APN reciprocally decreased after AD onset, indicating a possibility of APN contribution to protect a diseased aortic wall of AD.
Author Disclosures: Y. Watanabe: None. S. Miyagawa: None. S. Fukushima: None. N. Maeda: None. A. Saito: None. K. Torikai: None. K. Toda: None. T. Kuratani: None. I. Shimomura: None. Y. Sawa: None.
- © 2014 by American Heart Association, Inc.