Mechanism of Talibin-1 regulating vascular remodeling of aortic dissection in mice / 中华普通外科杂志

ABSTRACT

Objective:To explore the role and mechanism of Talin-1 in mouse aortic dissection.Methods:Sixty male FVB mice were evenly divided into groups of blank, model, Talin-1 up-regulation, Talin-1 up-regulation control, Talin-1 down-regulation, and Talin-1 down-regulation control. Except mice in the blank group, mice were treated with β-aminopropionitrile (BAPN) combined with angiotensin to construct a mouse aortic dissection model. Hematoxylin-eosin and vascular elastic fiber staining (EVG) were used to observe the aorta and elastic fiber morphology and structure. Western blot was used to detect the phosphorylation levels of FAK and ERK1 / 2 in mouse aortic tissue.Results:The success rate of aortic dissection in model mice was 70%, and there was no aortic dissection appeared in the blank group.No mice died during the experiment. The incidence of aortic dissection in the Talin-1 down-regulated group was 100%, which was significantly higher than that in the Talin-1 down-regulated control group( P<0.05). The incidence of aortic dissection in the Talin-1 up-regulated group was 20%, significantly lower than that in the Talin-1 up-regulated control group. The wall thickness of the aorta of mice in the Talin-1 down-regulated group was accompanied by hematoma or pseudocavity formation. The median elastic fiber content was higher than that in the Talin-1 downregulation control group( P<0.05). The content of elastic fibers in the blood vessel wall of mice in the Talin-1 up-regulation group was significantly higher than that in the Talin-1 up-regulation control group.The down-regulation of Talin-1 significantly inhibited FAK phosphorylation, and instead promoted ERK1/2 phosphorylation( P<0.05). Conclusions:Down-regulation of Talin-1 may reduce the elastic fiber content in the aorta of mice by activating the ERK1/2 signaling pathway, leading to vascular remodeling of the aortic wall and promoting the occurrence of aortic dissection.