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RESEARCH PRODUCT
Serum brain-derived neurotrophic factor and platelet activation evaluated by soluble P-selectin and soluble CD-40-ligand in patients with acute myocardial infarction
Emmanuel De MaistreJuliane BerchoudYannick BéjotPierre SicardAnne-cécile LagrostSébastien AmoureuxLuc RochetteMarianne ZellerLuc LorgisCatherine VergelyYves CottinAnnabelle Sequeira-le Grandsubject
PharmacologyBrain-derived neurotrophic factor0303 health sciencesmedicine.medical_specialtyP-selectinUnstable anginabusiness.industry030204 cardiovascular system & hematologymedicine.disease03 medical and health sciencesCoronary circulation0302 clinical medicineNerve growth factorEndocrinologymedicine.anatomical_structureNeurotrophic factorsInternal medicineImmunologymedicinePharmacology (medical)Platelet activationMyocardial infarctionbusiness030304 developmental biologydescription
Little is known about the role of neurotrophins (NT) under adult vascular homeostasis in normal and pathological conditions. The NT family, including nerve growth factor and brain-derived neurotrophic factor (BDNF) are expressed in atherosclerotic vessels. Previous studies demonstrated that plasma BDNF levels were increased in the coronary circulation in patients with unstable angina. However, the role of BDNF during the onset and evolution of unstable angina remains to be elucidated. The objective of this study was to evaluate the relationship between BDNF, functional parameters and biological markers associated with inflammatory processes and platelet activation. BDNF serum levels were assessed in patients with acute myocardial infarction (MI) (n = 20) or stable angina pectoris (SAP) (n = 20) who underwent coronary angiography. Serum levels of IL-6, MCP1, sVCAM, soluble CD-40-ligand (sCD40L) and soluble P-selectin (sP-selectin) were measured simultaneously by flux cytometry. Median BDNF levels were higher in the MI than in the SAP group (1730 vs. 877 pg/mL, respectively; P = 0.025). In MI patients, we observed a significant correlation between BDNF and sP-selectin (r = 0.58, P = 0.023), although we found a non-significant trend between BDNF and sCD40L (r = +0.35, P = 0.144). By contrast, no such correlation was observed in SAP patients (r = -0.22, P = 0.425). No difference was observed between the two groups regarding baseline demographics, risk factors, biological data and angiographic findings. The study suggests that BDNF serum levels in MI patients could be related to platelet activation and the inflammatory response. Further studies are needed to investigate the role of NT in the setting of acute MI.
year | journal | country | edition | language |
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2009-11-10 | Fundamental & Clinical Pharmacology |