Expression of genes encoding kinin receptors in peripheral blood mononuclear cells from patients with acute coronary syndromes
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Updated: Jun 26, 2026

Coronary Progenitor Cells and Soluble Biomarkers in Cardiovascular Prognosis after Coronary Angioplasty
Published on: January 28, 2020
1Department of Cardiology, Medical University of Silesia, Katowice, Poland.
Insights
Patients with acute coronary syndrome (ACS) exhibit an altered B1 receptor/B2 receptor ratio, suggesting a role for kinin signaling in the disease process. This imbalance may indicate increased activation of immune cells involved in atherosclerosis.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Immunology
Background:
- Inflammation is central to atherosclerosis, from plaque development to rupture causing acute coronary syndromes (ACS) like unstable angina (UA) and myocardial infarction (MI).
- Kinins, peptides mediating inflammation and vasodilation, act via B1 and B2 receptors, but their specific role in ACS remains unclear.
Purpose of the Study:
- To investigate the gene expression of B1 and B2 kinin receptors in patients diagnosed with ACS.
- To determine if kinin receptor expression patterns differ between ACS patients and healthy individuals.
Main Methods:
- Quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) was used to measure mRNA levels.
- Total mRNA was extracted from peripheral blood mononuclear cells of 40 ACS patients and 10 healthy controls.
- The ratio of B1 receptor (B1R) to B2 receptor (B2R) mRNA was calculated and compared between groups.
Main Results:
- ACS patients displayed an inverted B1R/B2R ratio compared to healthy controls (P < 0.01 for MI vs C; P < 0.05 for UA vs C).
- A significant decrease in B2R mRNA levels was observed in the MI group compared to controls (P < 0.05).
- No significant differences in B1R expression were found between MI and control groups, nor were differences observed in B1R or B2R expression between UA and control groups.
Conclusions:
- Patients with ACS present with an altered B1R/B2R ratio, indicating a potential disruption in kinin signaling pathways.
- This disturbed kinin signaling may be linked to heightened activation of circulating mononuclear cells, which are key players in atherosclerotic plaque progression and rupture.
Background:
Inflammation plays a critical role in all stages of atherogenesis, including plaque destabilization leading to the rupture and local thrombosis, clinically manifested as unstable angina (UA) or myocardial infarction (MI). Recent data report enhanced expression of numerous pro-inflammatory genes in patients with acute coronary syndrome (ACS) both in plaque and in inflammatory cells. Kinins are peptides involved in vasodilation, vascular permeability, pain and inflammation. Their effects are mediated by two receptors, B1 and B2. As the role of kinins in ACS is not clear, the aim of the study was to assess the expression of the genes encoding kinin receptors in patients with ACS.
Methods:
The study was carried out on 40 patients with ACS and 10 age-matched healthy subjects (control (C)). To evaluate gene expression of B1 and B2 kinin receptors, total mRNA was extracted from peripheral blood mononuclear cells and the number of mRNA copies was assessed by quantitative reverse transcriptase-polymerase chain reaction.
Results:
In patients with MI and UA, the B1 receptor (B1R)/B2 receptor (B2R) ratio was inversed compared with healthy subjects (C group) (MI vs C: 1.54 +/- 0.39 vs 0.36 +/- 0.04; P < 0.01; UA vs C: 2.13 +/- 0.98 vs 0.36 +/- 0.04; P < 0.05 respectively). B2R gene mRNA level was markedly lower in MI group versus C group (24 216 +/- 5409 copies/microg vs 39 908 +/- 5309 copies/microg; P < 0.05). The difference in B1R gene expression between MI and C group was negligible. We have not observed differences in studied genes expression between UA and C groups.
Conclusion:
Patients with ACS show inverted B1R/B2R ratio. Such disturbance in kinin signalling may reflect increased activation of circulating mononuclears, which are important participants of atherosclerotic plaque development and eventually rupture.
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