No abstract

No abstract

Background: Thrombosis triggered by platelet activation plays a vital role in the pathogenesis of cardiovascular and cerebrovascular diseases. Objective: To find platelet combined biomarkers for cardiovascular diseases and investigate the possibility of Concanavalin A (ConA) acting on platelets as a new pharmacological target. Methods: High-throughput Technology and bioinformatics analysis were combined and groups of microarray chip gene expression profiles for acute myocardial infarction (AMI) and sickle cell disease (SCD) were obtained using GEO database screening. R language limma package was used to obtain differentially expressed genes (DEGs). GO, KEGG and other databases were utilized to perform the enrichment analysis of DEGs functions, pathways, etc., PPI network was constructed using STRING database and Cytoscape software, and MCC algorithm was used to obtain the 200 core genes of the two groups of DEGs. Core targets were confirmed by constructing an intersection area screening. A type of molecular probe ConA was molecularly docked with the above core targets on the Zdock, HEX and 3D-DOCK servers. Result: we found six core markers CD34, SOCS2, ABL1, MTOR, VEGFA, and SMURF1 which were simultaneously related to both diseases, and the docking effect showed that VEGFA is the best-performing. Conclusion: VEGFA is most likely to reduce its expression by binding to ConA, which could affect the downstream regulation of the PI3K/Akt signaling pathway during platelet activation. Some other core targets also have the opportunity to interact with ConA to affect platelet-activated thrombosis and trigger changes in cardiovascular events.

No abstract