Abstract
Cerebrovascular disease is currently a serious threat to human health and life, commonly including cerebral infarction, cerebral hemorrhage and transient cerebral ischemia, among others. To explore the role and e molecular mechanism of GP6 in the development of cerebral ischemic stroke (CIS) induced by atherosclerosis (AS). Forty-five male New Zealand white rabbits were randomly divided into 3 groups: the control, CIS model and anti-GP6 group. Carotid artery tissues and blood of the white rabbits were collected for analysis. Hematoxylin and eosin (H&E) staining was used to analyze the pathological characteristics of vascular endothelial injury. Flow cytometry (FCM) was performed to analyze the content of Th1 and Th17 in blood. Immunohistochemistry was used to analyze the distribution and relative expression of FCER1G, ITGA2 and GP6 proteins in the carotid artery and cerebrovascular tissues. Western blot was applied to determine the protein expression of GP6, FYN, PKA, pPTK2, and pFAK1 in carotid artery tissues of the rabbits. In the CIS model group, there was lymphocyte infiltration, fibrous tissue formation, and the formation of thrombus and lipid plaques. In the anti-GP6 group, scattered thin plaques were observed, and no obvious foam cell deposition was observed. The Th1 and Th17 content was significantly decreased in the CIS model group compared to the control and anti-GP6 group. The relative expression of FCER1G, ITGA2 and GP6 in the CIS model group was significantly higher compared to those in the control group and anti-GP6 group. The protein expression of GP6, FYN, PKA, pPTK2, and pFAK1 in the CIS model group were markedly higher compared to those in the control group and anti-GP6 group. GP6 can promote the development of CIS by activating the FYN-PKA-pPTK2/FAK1 signaling pathway.
Highlights
Cerebrovascular disease is currently a serious threat to human health and life, commonly including cerebral infarction, cerebral hemorrhage and transient cerebral ischemia, among others
glycoprotein 6 (GP6) can promote the development of cerebral ischemic stroke (CIS) by activating the FYN-protein kinase A (PKA)-pPTK2/FAK1 signaling pathway
Carotid artery tissue and cerebrovascular tissues were collected from the white rabbits, and Hematoxylin and eosin (H&E) staining was used to analyze the pathological characteristics of the vascular endothelial injury
Summary
Cerebrovascular disease is currently a serious threat to human health and life, commonly including cerebral infarction, cerebral hemorrhage and transient cerebral ischemia, among others. How to prevent and treat cerebrovascular disease more effectively is the most serious problem that neurology faces presently.[5] Cerebral ischemic stroke (CIS) is ischemic necrosis or softening of localized brain tissue due to cerebral blood circulation disorder, ischemia or hypoxia. It is the most common type of cerebrovascular disease, accounting for about 70% of all acute cerebrovascular diseases. About 30–40% of CIS is caused by carotid atherosclerotic stenosis.[6]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
