Abstract
The pathogenesis of abdominal aortic aneurysm (AAA) is characterized to be inflammation-associated degeneration of vascular wall. Neovascularization is regularly found in human AAA and considered to play critical roles in the development and rupture of AAA. However, little is known about lymphangiogenesis in AAA. The purpose of this study was to demonstrate both angiogenesis and lymphangiogenesis in AAA. Abdominal aortic tissue was harvested either from autopsy (control group) and during open-repair surgery for AAA (AAA group). Adventitial lymphatic vasa vasorum was observed in both groups, but seemed to be no significant morphological changes in AAA. Immunohistochemical studies identified infiltration of lymphatic vessel endothelial hyaluronan receptor (LYVE) −1, vascular endothelial growth factor (VEGF)-C, and matrix metalloproteinase (MMP)-9-positive macrophages and podoplanin and Prox-1-positive microvessels in the intima/media in AAA wall, where hypoxia-inducible factors (HIF)-1α was expressed. VEGF-C and MMP-9 were not expressed in macrophages infiltrating in the adventitia. Intraoperative indocyanine green fluorescence lymphography revealed lymph stasis in intima/medial in AAA. Fluorescence microscopy of the collected samples also confirmed the accumulation of lymph in the intima/media but not in adventitia. These results demonstrate that infiltration of macrophages in intima/media is associated with lymphangiogenesis and angiogenesis in AAA. Lymph-drainage appeared to be insufficient in the AAA wall.
Highlights
Abdominal aortic aneurysm (AAA) is a common disease among elderly people
We investigated the presence of lymphanagiogenesis and major drivers of angiogenesis and lymphangiogenesis such as vascular endothelial growth factor (VEGF)-A and VEGF-C in abdominal aortic aneurysm (AAA) wall using AAA samples which were obtained during open repair of AAA surgery
We demonstrated the presence of adventitial LVV in both autopsied normal aorta and AAA
Summary
Abdominal aortic aneurysm (AAA) is a common disease among elderly people. AAA affects 5–10% of men over 65 years and is the tenth leading cause of death in men over the age of 55 years in the United States [1]. The degeneration of vascular wall has been considered as one of the main causes of AAA onset and rupture. Previous studies have demonstrated infiltration of inflammatory cells, such as macrophages, T cells, neutrophils and dendric cells, into the aortic wall [2,3] These inflammatory cells are considered to contribute to the pathogenesis of AAA through the secretion of inflammatory mediators, including cytokines, chemokines, and MMPs [4]. We have recently demonstrated the arteriosclerotic degeneration of VV and tissue ischemia in AAA wall [5]. These inflammatory and hypoxic environment are potential stimuli for angiogenesis as previously reported [6]. We investigated the presence of lymphanagiogenesis and major drivers of angiogenesis and lymphangiogenesis such as VEGF-A and VEGF-C in AAA wall using AAA samples which were obtained during open repair of AAA surgery
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