[Role of mimecan in development of atherosclerosis induced by increased blood pressure variability]

To examine the changes of mimecan protein expression in development of atherosclerosis induced by sinoaortic denervation, and to explore the effects of mimecan knock down on the proliferation and migration of vascular smooth muscle cells.
 Methods: The animals were randomly divided into a sham group and a model group (n=8 in each group). The rat model of blood pressure variability was established by sinoaortic denervation, and the hemodynamic indexes were recorded 20 weeks after the surgery to confirm the success of the model. The thoracic aorta was excised and stained with immunohistochemistry to observe the pathological changes of smooth muscle tissues and the changes of mimecan expression. The mice vascular smooth muscle cells were isolated, and which were treated with mimecan siRNA to knock down the mimecan expression. The cell proliferation was observed by 5-ethynyl-2'-deoxyuridine (Edu) in corporation test and the changes of cell migration was observed by wound healing test.
 Results: Twenty weeks after sinoaortic denervation, the blood pressure variability in the model group was significantly increased compared with that in the sham group, suggesting the model was successfully established. In addition, the increased blood pressure variability in the model group promoted the proliferation and migration of the vascular smooth muscle cells in thoracic aorta, while the expression of mimecan protein was significantly decreased. In in vitro assays, the knock down of mimecan in mice vascular smooth muscle cells could promote the cell proliferation and migration.
 Conclusion: Mimecan plays a protective role in the development of sinoaortic denervation induced atherosclerosis through amechanism involving suppression of the proliferation and migration of vascular smooth muscle cells.