Aortic adventitial angiogenesis and lymphangiogenesis promote intimal inflammation and hyperplasia

Introduction itial inflammation is known to influence neointimal formation and vascular remodeling. The present study was aimed to clarify the relationship between neointima hyperplasia and adventitial angiogenesis and lymphangiogenesis after balloon-induced aortic endothelial injury. s y male Wistar rats were randomly divided into six interventional groups and one control group. The intimal area/medial area ratio (I/M ratio), the adventitial macrophage index, and the number of adventitial microvessels (Ad-MV) and lymphatic vessels (Ad-LV) in the aorta were measured, and the mRNA expressions of VEGF-A, VEGFR-1, VEGF-C, VEGFR-3, PDGF-B, and PDGFR-β in the aortic wall were quantified by real-time RT-PCR. s ed with the control group, the I/M ratio, macrophage index, Ad-MV, Ad-LV, and the mRNA expressions of VEGF-A, VEGFR-1, VEGF-C, VEGFR-3, PDGF-B, and PDGFR-β in interventional groups increased significantly after balloon-induced injury. I/M ratio showed significant correlations with Ad-MV and Ad-LV after balloon intervention. Multiple linear regression analysis indicated that Ad-MV and Ad-LV were independent factors of intimal hyperplasia. sion itial angiogenesis and lymphangiogenesis are induced by intimal inflammation after balloon injury, and these neogenetic vessels in turn promote intimal inflammation and hyperplasia probably via delivery and activation of inflammatory cells.