Odels underline that circulating EPC-based therapy: (i) have the ability to improve plasmatic and hemodynamic parameters; (ii) reduced platelet activation and modulated their pro-inflammatory and thrombogenic properties during atherosclerotic process; (iii) in combination with PMPs have several beneficial effects on platelet function, but no better than in situation without microparticles. Although, some studies reported that PMPs enhance the potential of EPCs to restore endothelial integrity after vascular injury [53], while PMP injections were sufficient to stimulate postischemic revascularization in the myocardium, in a rat model of chronic myocardial ischemia [54], our results suggested that PMPs did not improve the EPC effects on the platelet activation induced by hypertension associated with hypercholesterolemia. This study reveals a new biological role for circulating EPCs in regulation of platelet function in atherosclerosis. However, the existence of a cross talk order Asiaticoside A between EPCs and platelets, in each other’s function regulation, requires future studies to explore the interactions between these cells and the mechanisms that underlie this relationship in vascular repair and atherosclerosis.AcknowledgmentsThe authors gratefully acknowledge and appreciate the dedicated work and help of the technicians Marilena Isachi, Marcela Toader (biochemistry), and Safta Nae (experimental models).Author ContributionsPerformed the experiments: AG. Analyzed the data: NA. Wrote the paper: NA. Designed the study, performed the statistical analysis, interpreted the data: NA AG. Critical revision of the manuscript for important intellectual contect: DP AG. Effectively participated at the realization of the experimental models: ED. Substantial contribution to the acquisition of the data for flow cytometry: EA. Substantial contributions to the acquisition of the data: AG.
Despite recent advances in medical and interventional treatment strategies coronary artery disease (CAD) remains the leading cause of myocardial infarction and sudden cardiac death in industrialized countries[1,2]. In patients with acute myocardial infarction, the rupture of coronary plaques with initiation of thrombus formation and subsequent embolization of atherosclerotic debris result in myocardial cell necrosis. However, atherosclerotic plaque development occurs `silently’ over several decades before the clinical manifestation of acute coronary syndromes[3,4].Currently, AN-3199 manufacturer non-invasive imaging of coronary vessels is feasible using coronary computed tomography angiography (CCTA), which allows the evaluation of the coronary vessel wall, in addition to the assessment of coronary lumen narrowing[5]. Such characterization of coronary atherosclerotic lesions was shown to have incremental value for the assessment of cardiovascular risk and prediction of future cardiac events compared to clinical parameters and coronary calcification[6?]. Biochemical markers on the other hand, can be easily acquired and can help understanding the underlying pathophysiology of coronary atherosclerosis development and progression. In this regard, we recently demonstrated that high mobility group boxHMGB1 and Atherosclerotic Plaque Composition(HMGB1, also known as amphoterin) protein is a critical mediator of in acute experimental ischemic injury[9] and predicts outcome after myocardial infarction[10]. In addition, we and others recently reported that high sensitive troponin T (hs-TnT), a well established marker.Odels underline that circulating EPC-based therapy: (i) have the ability to improve plasmatic and hemodynamic parameters; (ii) reduced platelet activation and modulated their pro-inflammatory and thrombogenic properties during atherosclerotic process; (iii) in combination with PMPs have several beneficial effects on platelet function, but no better than in situation without microparticles. Although, some studies reported that PMPs enhance the potential of EPCs to restore endothelial integrity after vascular injury [53], while PMP injections were sufficient to stimulate postischemic revascularization in the myocardium, in a rat model of chronic myocardial ischemia [54], our results suggested that PMPs did not improve the EPC effects on the platelet activation induced by hypertension associated with hypercholesterolemia. This study reveals a new biological role for circulating EPCs in regulation of platelet function in atherosclerosis. However, the existence of a cross talk between EPCs and platelets, in each other’s function regulation, requires future studies to explore the interactions between these cells and the mechanisms that underlie this relationship in vascular repair and atherosclerosis.AcknowledgmentsThe authors gratefully acknowledge and appreciate the dedicated work and help of the technicians Marilena Isachi, Marcela Toader (biochemistry), and Safta Nae (experimental models).Author ContributionsPerformed the experiments: AG. Analyzed the data: NA. Wrote the paper: NA. Designed the study, performed the statistical analysis, interpreted the data: NA AG. Critical revision of the manuscript for important intellectual contect: DP AG. Effectively participated at the realization of the experimental models: ED. Substantial contribution to the acquisition of the data for flow cytometry: EA. Substantial contributions to the acquisition of the data: AG.
Despite recent advances in medical and interventional treatment strategies coronary artery disease (CAD) remains the leading cause of myocardial infarction and sudden cardiac death in industrialized countries[1,2]. In patients with acute myocardial infarction, the rupture of coronary plaques with initiation of thrombus formation and subsequent embolization of atherosclerotic debris result in myocardial cell necrosis. However, atherosclerotic plaque development occurs `silently’ over several decades before the clinical manifestation of acute coronary syndromes[3,4].Currently, non-invasive imaging of coronary vessels is feasible using coronary computed tomography angiography (CCTA), which allows the evaluation of the coronary vessel wall, in addition to the assessment of coronary lumen narrowing[5]. Such characterization of coronary atherosclerotic lesions was shown to have incremental value for the assessment of cardiovascular risk and prediction of future cardiac events compared to clinical parameters and coronary calcification[6?]. Biochemical markers on the other hand, can be easily acquired and can help understanding the underlying pathophysiology of coronary atherosclerosis development and progression. In this regard, we recently demonstrated that high mobility group boxHMGB1 and Atherosclerotic Plaque Composition(HMGB1, also known as amphoterin) protein is a critical mediator of in acute experimental ischemic injury[9] and predicts outcome after myocardial infarction[10]. In addition, we and others recently reported that high sensitive troponin T (hs-TnT), a well established marker.
