AI Article Synopsis
- The TRPV2 channel is found to be upregulated in certain immune cells following an acute myocardial infarction (AMI), but this overexpression might hinder heart recovery.
- Researchers tested TRPV2 levels in blood samples from AMI patients compared to those with healthy coronary arteries, examining its relationships with various inflammatory and cardiac markers.
- Results indicated lower TRPV2 expression in AMI patients and showed that this expression inversely correlated with inflammation markers like CRP and troponin I, suggesting TRPV2 could be a new target for potential heart treatments after an MI.
Article Abstract
Objectives: We have recently shown that the transient receptor potential vanilloid 2 (TRPV2) channel is exclusively upregulated in rat/murine peri-infarct monocytes/macrophages following an acute myocardial infarction (AMI), and that this overexpression might be detrimental for cardiac recovery. We aimed to characterize the expression levels of TRPV2 in peripheral blood mononuclear cells (PBMCs) of AMI patients relative to individuals with normal coronaries, and to analyze potential associations with inflammatory and cardiac ischemic markers.
Methods: Patients who underwent coronary angiography due to AMI or chest pain were prospectively included. PBMCs were isolated from whole blood by Ficoll gradient centrifugation. TRPV2 expression was analyzed by real-time PCR. C-reactive protein (CRP) and troponin I (TpI) levels were determined at the central chemistry laboratory; interleukin 6 and insulin-like growth factor (IGF)-1 levels were tested by ELISA.
Results: Following AMI, the number of TRPV2-expressing PBMCs was reduced when compared to in patients with normal coronaries. An inverse correlation was documented between the numbers of circulating macrophages and TRPV2 expression. Additionally, TRPV2 expression was inversely correlated with CRP and TpI and directly correlated with serum IGF-1.
Conclusions: We assume that peripheral TRPV2 downregulation occurs concomitantly with the accumulation of TRPV2-white blood cells in the peri-infarct zone. TRPV2 may thus represent a novel target for treatment in the acute phase after MI.
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| http://dx.doi.org/10.1159/000486530 | DOI Listing |
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