Abstract
This study aimed to explore the role of clusterin released by platelet aggregation in restenosis after carotid endarterectomy. 35 patients who underwent carotid endarterectomy due to carotid artery stenosis were enrolled in this study. They were admitted to the Third Affiliated Hospital of Qiqihar Medical University from January 2018 to January 2019. All the patients were divided into two groups: the restenosis group and the nonrestenosis group, according to the follow-up results within 12 months. Peripheral blood was collected on the first day, 6 months, and 12 months after operation. The expression of CLU in serum of plasma and platelet culture medium was detected by an ELISA experiment. The vascular endothelial cells were cultured in vitro with 100 ng/mL of human recombinant CLU added to the medium. Cell proliferation, migration, and invasion were detected by CCK8, scratch, and Transwell invasion tests. The expression level of TLR3 and NF-κb p65 proteins in cells was detected by western blot. TLR3 knockout plasmids in vascular endothelial cell lines were transfected. Cell proliferation and migration were detected by CCK8 and the scratch assay. The CLU content in peripheral blood plasma and supernatant of platelet culture medium was significantly higher in the restenosis group than that of the control group (p=0.003) 6 months after operation (p=0.047) and 12 months after operation (p=0.011). When CLU was added to vascular endothelial cell culture medium, the proliferation and migration were significantly enhanced. The TLR3/NF-κb p65 protein expression level in cells also significantly increased. After the transfection of TLR3 knockout plasmids into vascular endothelial cell lines, CLU cannot promote the proliferation and migration of vascular endothelial cells. Platelet-released clusterin can induce vascular endothelial cell proliferation and migration by activating the TLR3/NF-kb p65 signaling pathway, leading to carotid artery restenosis after carotid endarterectomy.
Highlights
Carotid artery stenosis is one of the important factors leading to ischemic stroke [1]. e current global incidence is about 4.4%–7%, of which about 25%–30% of rigid artery stenosis is closely related to stroke [2]
Atherosclerosis in the neck is a common cause of this disease. e intima and plate of the lesion can be removed by carotid endarterectomy (CEA), a minimally invasive surgery, and the arterial anatomical passage can be restored
Research Subjects. 35 patients who underwent carotid endarterectomy due to carotid artery stenosis were enrolled in this study. ey were admitted to the Department of Vascular Surgery, the ird Affiliated Hospital of Qiqihar Medical University, from January 2018 to January 2019. ere were 21 males and 14 females, aged 48–69 years with an average age of
Summary
Carotid artery stenosis is one of the important factors leading to ischemic stroke [1]. e current global incidence is about 4.4%–7%, of which about 25%–30% of rigid artery stenosis is closely related to stroke [2]. Carotid artery stenosis is one of the important factors leading to ischemic stroke [1]. CEA has been proven to be effective in treating carotid artery stenosis and preventing ischemic stroke [3]. The treatment may cause a variety of complications, including surgery-related deaths, ischemic stroke, myocardial infarction, overperfusion syndrome, and postoperative restenosis [4, 5]. Yuichi et al [6] found that the incidence of restenosis in patients with high platelet aggregation scores was significantly higher than that in patients with low scores, which could be an important and effective index to predict restenosis after CEA operation. Studies have shown that platelet aggregation leads to the release of clusterin (CLU), which plays an important role in many cardiovascular and cerebrovascular diseases, such as cerebral amyloid angiopathy, atherosclerosis, and stenosis [7,8,9]. There have been few studies on the mechanism of how it affects the prognosis of patients after carotid endarterectomy
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