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Updated: Feb 22, 2026

Methods for Quantitative Detection of Antibody-induced Complement Activation on Red Blood Cells
Published on: January 29, 2014
Evaluation of expression levels and mechanism of complement activation
Xing Wang1, An-Heng Liu2, Zhong-Wei Jia1
1Department of Cardiology, The 254th Hospital of PLA, Tianjin 300142, P.R. China.
Insights
Complement system activation and elevated C3a receptor expression occur in acute myocardial infarction (AMI). This suggests the C3a-C3a receptor pathway may contribute to heart attack development.
Area of Science:
- Cardiovascular Medicine
- Immunology
- Molecular Biology
Background:
- Acute myocardial infarction (AMI) involves complex inflammatory processes.
- The role of the complement system in AMI pathogenesis requires further elucidation.
Purpose of the Study:
- To investigate complement system activation during AMI.
- To determine the expression levels of the C3a receptor in myocardial infarction tissues.
Main Methods:
- Plasma levels of complement activation products (C3a, C4a, C5a) were measured using cytometric bead array.
- C3a receptor protein expression in cardiac tissues was assessed via immunoblotting.
- Study included healthy individuals and patients with coronary artery stenosis or AMI.
Main Results:
- Significantly elevated levels of C3a, C4a, and C5a were observed in patients with coronary artery stenosis and AMI compared to controls (P<0.01).
- Protein expression of the C3a receptor was significantly higher in infarct tissues from AMI patients than in adjacent normal tissues (P<0.05).
Conclusions:
- Complement system activation is evident in patients with acute myocardial infarction.
- Increased C3a receptor expression in infarct zones suggests the C3a-C3a receptor pathway's involvement in myocardial infarction development.
Abstract:
The present study aimed to reveal the expression changes of complement system activation and complement activation product C3a receptor during acute myocardial infarction. Blood samples were collected from healthy individuals and from patients with coronary artery stenosis or acute myocardial infarction. The subjects received physical examination in hospital between January and July 2015 (n=5). Cytometric bead array was performed to measure the levels of complement system activation product anaphylatoxin C3a, C4a and C5a. Immunohistochemical investigations were performed in tissues of patients who underwent coronary artery bypass grafting between January and July 2015 to detect the expression of C3a receptor. The results of cytometric bead array showed that the content of complement activation products C3a, C4a and C5a in the plasma of patients with coronary artery stenosis and acute myocardial infarction were significantly higher than those of the control group (P<0.01). The results of immunoblotting suggested that the protein expression of C3a receptor in infarct tissues of patients with acute myocardial infarction was significantly higher than that of normal tissues adjacent to the infarcted area (P<0.05). There is complement system activation in patients with acute myocardial infarction. Additionally, the increase in the expression of complement C3a receptor in tissues of infarct area suggested that C3a-C3a receptor signaling pathway may be involved in the development of myocardial infarction.
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