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Updated: Oct 28, 2025
Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation
Published on: May 23, 2025
Study on the interaction mechanism between C-reactive protein and platelets in the development of acute myocardial
Yubao Liu1, Shuhui Lai2, Lijie Liang3
1Department of Intensive Care Medicine, The Second Affiliated Hospital of Qiqihar Medical College, Qiqihar, China.
Background:
Myocardial 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.
Methods:
We 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.
Results:
Gene 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).
Conclusions:
From 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.
Insights
Platelet gene expression after myocardial infarction (MI) reveals C-reactive protein (CRP) increases, activating platelets. This suggests platelets may play an anti-inflammatory role in acute MI (AMI) development.
Area of Science:
- Cardiovascular Biology
- Platelet Genomics
- Biomedical Research
Background:
- Myocardial infarction (MI) is a critical cardiovascular event where platelets play a key role.
- Platelets, lacking nuclear DNA, retain mRNA, offering insights into pre-coronary event mechanisms.
- The precise role of platelet transcriptome in acute myocardial infarction (AMI) remains unclear.
Purpose of the Study:
- To investigate platelet gene expression following the first AMI event.
- To elucidate the mechanisms of platelet involvement in AMI pathogenesis using bioinformatics and animal models.
Main Methods:
- Acquired platelet gene expression data from AMI patients via Gene Expression Omnibus (GEO).
- Identified differentially expressed genes (DEGs) using R language and performed Weighted Gene Co-expression Network Analysis (WGCNA).
- Utilized in vivo AMI rat models to validate bioinformatics findings.
Main Results:
- Identified 2,852 DEGs (P<0.05, |log2FC| >1) in platelets post-AMI.
- Found a significant association between C-reactive protein (CRP) and Staphylococcus aureus infection (SAI).
- Observed elevated CRP levels in AMI rats, with increased FCGR2B mRNA and HLA-DRB4 mRNA expression.
Conclusions:
- Increased CRP levels in AMI may activate platelets.
- Platelet activation by CRP suggests a potential anti-inflammatory role in AMI development.
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