Study on the interaction mechanism between C-reactive protein and platelets in the development of acute myocardial infarction.

Abstract

BackgroundMyocardial infarction (MI) is the single most critical event in coronary disease. Platelets are involved in the processes of acute MI (AMI). They lack nuclear DNA but retain megakaryocyte mRNAs, hence, their transcriptome could provide information preceding coronary events. However, their mechanisms are not clear. In this study, we obtained a gene expression atlas of platelets from patients after their very first AMI, and our purpose was to clarify the mechanisms of platelet involvement in the occurrence of AMI through bioinformatics analyses and animal models of AMI in vivo.MethodsWe obtained a gene expression atlas of platelets from patients after their very first AMI from the Gene Expression Omnibus (GEO). Differentially expressed genes (DEGs) were retrieved using R language. Weighted gene co-expression network analysis (WGCNA) was implemented in order to construct a gene co-expression correlation network among DEGs. Animal models of AMI in vivo were constructed to confirm the results of the bioinformatics analysis.ResultsGene integration analysis yielded 2,852 DEGs (P<0.05, |log2FC| >1). Bioinformatics analysis demonstrated a significant association between C-reactive protein (CRP) and Staphylococcus aureus infection (SAI) (P=0.015). Data from in vivo experiments showed that CRP increased significantly in AMI rats (P<0.001), and the expression of FCGR2B mRNA and HLA-DRB4 mRNA was elevated in response to the increase of CRP (P<0.001).ConclusionsFrom the results of this study, we speculate that in the development of AMI, the increase in CRP activates platelets and induces platelets to play an anti-inflammatory role.