%0 Journal Article
%T Expression and Function of Ephrin-B1 and Its Cognate Receptor EphB2 in Human Abdominal Aortic Aneurysm
%A Aiji Sakamoto
%A Masaaki Kawashiri
%A Hatsue Ishibashi-Ueda
%A Yuka Sugamoto
%A Tsuyoshi Yoshimuta
%A Takeo Higashikata
%A Hitoshi Ogino
%A Hayato Tada
%A Tetsuo Konno
%A Kenshi Hayashi
%A Masakazu Yamagishi
%J International Journal of Vascular Medicine
%D 2012
%I Hindawi Publishing Corporation
%R 10.1155/2012/127149
%X We examined the expression of ephrin-B1 and its cognate receptor EphB2, key regulators of angiogenesis and embryogenesis, in human abdominal aortic aneurysm (AAA) and analyzed their functional roles in cell migration. From 10 patients (9 males and 1 female; age, ) who underwent vascular surgery for AAA, we obtained AAA and adjacent control tissues. Using real-time RT-PCR, we analyzed expression of ephrin-B1 and EphB2. We also histologically localized these molecules in AAA tissues. Finally, effects of ephrin-B1 and EphB2 on inflammatory cell chemotaxis were examined by cell migration assay. Expression levels of ephrin-B1 ( versus , ) and EphB2 ( versus , ) were higher in AAA than normal control. Both ephrin-B1 and EphB2 were expressed in macrophages, T lymphocytes, and endothelial cells within AAA. In chemotaxis assay, ephrin-B1 and EphB2 inhibited mononuclear-cell chemotaxis induced by stromal derived factor-1 down to % ( ) and % ( ), respectively. These data suggest that ephrin-B1 and EphB2 might be functional in human adult inflammatory cells and involved in the pathogenesis of AAA, although specific roles of these molecules should further be sought. 1. Introduction Abdominal aortic aneurysm (AAA) has high risk for aortic rupture and constitutes one of the major causes of elderly death [1], sometimes being associated with coronary ectasia [2]. Compared to occlusive atherosclerosis such as carotid atheroma, AAA affects much more extensive layers of blood vessels but shares some pathogenic aspects such as inflammatory cell accumulation [3]. Genetically engineered mouse models for AAA have elucidated key molecules for the pathogenesis of AAA [4]. For example, some matrix metalloproteinases (MMPs) are upregulated and expressed in macrophages within AAA, which is likely to cause medial degeneration in AAA [5] with or without physiological stress such as hypoxia [6]. However, our understanding on the molecular and cellular pathogenesis of AAA is still limited, especially in cases of humans. Recently, we have found that ephrin-B1 and its cognate receptor EphB2, the key regulators of angiogenesis and embryogenesis, are upregulated and predominantly expressed in macrophages and T-lymphocytes in human carotid atherosclerotic plaque [6]. Ephrin-B1 and EphB2 belong to ephrin and Eph family of genes consisting 21 members, which are expressed ubiquitously in embryonic tissues and involved in morphogenesis by regulating cell adhesion and migration [7, 8]. Therefore, we hypothesized that ephrin-B1 and EphB2 might be also involved in the pathogenesis of AAA and set
%U http://www.hindawi.com/journals/ijvm/2012/127149/