Microvessels and glypican‐1 appears in atherosclerotic plaque in the aortic arch of aged rats

Abstract

Rupture of atherosclerotic plaque is a major cause of death in acute cardiovascular and cerebrovascular events. We believe that the growth of plaques leads to microcirculation dysfunction, which promotes angiogenesis for establishing a new microcirculation in pathological tissues to achieve new homeostasis. However, rupture of atherosclerotic plaque occurs during the establishment of new microcirculation. There is abundant neovascularization in ruptured atherosclerotic plaques. It was demonstrated that endothelial glycocalyx is required for angiogenesis, but their specific angiogenic mechanism remains unclear. In order to investigate the relationship between endothelial glycocalyx and the angiogenesis of atherosclerotic vulnerable plaque, we detected the aortic arch plaque in 23-month-old rats and performed the immunofluorescence staining of CD31 and glypican-1 in frozen sections of the aortic root and aortic arch. Then, the role of glypican-1 in angiogenesis induced by fluid shear stress was analyzed by in vitro experiments. Results showed that there are abundant microvessels in the atherosclerotic plaque of the aortic arch in aged rats, and there is a high level of glypican-1 in the atherosclerotic plaque. In vitro experiments showed that the shedding of glypican-1 by phosphatidylinositol-specific phospholipase C (PI-PLC) could inhibit 25 dyn/cm2 shear stress-induced angiogenesis, indicating that glypican-1 plays an important role in angiogenesis in atherosclerotic plaque. The relationship between glypican-1 and neovascularization, and their roles in atherosclerotic plaque rupture need further study.