Acquired CCN2 deficiency induces aortic elastic layer disruption that are more severe in Ang II-infused mice
To further determine the impact of CCN2 deficiency on aortic structure, aortic sections were first evaluated by histological techniques. In CCN2-KO mice infused with Ang II, aneurysmal lesions were characterized by elastic lamina rupture and aortic wall dissection with extravasation of red blood cells outside the muscle layer forming a neo-lumen. Aneurysms also presented inflammatory cell infiltration in the border of the dissected aortic wall, along with reduced cellularity of the muscular layer (Figure 4A ). Interestingly, Van Gieson staining revealed some areas with disruption of elastic layers in the aortic wall of CCN2-KO mice, both in untreated and Ang II-treated mice, as well as elastic layer thinning or absence in aortic aneurysm sections (Figure 4B, arrows).Ultrastructural electron microscopy studies of the aorta showed abnormalities in the elastic laminae. Thus, WT aortas displayed continuous elastic laminae with a consistent width, while CCN2-KO mice showed variable width and a disrupted architecture, including abnormal collagen distribution (Figure 4C ).