Abstract
BackgroundPlatelet aggregation mediated by inflammation played a critical role in the development of coronary heart diseases (CHD). Our previous clinical researches showed that Th17 cells and their characteristic cytokine IL-17A were associated with the plaque destabilization in patients with acute coronary syndrome (ACS). However, the potent effect of IL-17A on platelets-induced atherothrombosis remains unknown.Methods and ResultsIn this study, we detected the plasma IL-17A levels and platelet aggregation in patients with stable angina (SA), unstable angina (UA), acute myocardial infarction (AMI) and chest pain syndrome (CPS). In addition, the markers of platelet activation (CD62P/PAC-1) and the mitogen-activated protein kinases (MAPKs) pathway were detected in platelets from ACS patients. We found that plasma IL-17A levels and platelet aggregation in patients with ACS (UA and AMI) were significantly higher than patients with SA and CPS, and the plasma IL-17A levels were positively correlated with the platelet aggregation (R = 0.47, P<0.01). In addition, in patients with ACS, the platelet aggregation, CD62P/PAC-1 and the phosphorylation of ERK2 signaling pathway were obviously elevated in platelets pre-stimulated with IL-17A in vitro. Furthermore, the specific inhibitor of ERK2 could attenuate platelet aggregation and activation triggered by IL-17A.ConclusionOur experiment firstly proved that IL-17A could promote platelet function in patients with ACS via activating platelets ERK2 signaling pathway and may provide a novel target for antiplatelet therapies in CHD.
Highlights
Atherosclerosis is the primary cause of cardiovascular disease among adults worldwide [1]
Our experiment firstly proved that IL-17A could promote platelet function in patients with acute coronary syndrome (ACS) via activating platelets ERK2 signaling pathway and may provide a novel target for antiplatelet therapies in coronary heart diseases (CHD)
All participators were divided into 4 groups: (a) In the acute myocardial infarction (AMI) group (n = 10), patients showed significant rise of serum creatine kinase MB and troponin I, ischemia symptoms, or typical elecrocardiographic changes; (b) The unstable angina (UA) group (n = 15) included patients who suffered chest pain at rest with definite ST-segment change and/or T-wave inversions; (c) In stable angina (SA) group (n = 15), patients had effort angina accompanied by downsloping or horizontal ST-segment depression.1 mm in an exercise. (d) In chest pain syndrome (CPS) group (n = 14), chest pain without being accompanied by electrocardiographic changes, coronary artery stenosis
Summary
Atherosclerosis is the primary cause of cardiovascular disease among adults worldwide [1]. Platelet activation and aggregation triggered by inflammation on the ruptured atherosclerotic plaque is the critical mechanism in the development of atherosclerosis and its thrombotic complication [2,3,4,5]. We and others have reported that IL-17A was elevated in patients with acute coronary syndrome (ACS) and atherosclerosis animal models [9,10]. The relationship between IL-17A and platelets function remains unknown in coronary heart diseases (CHD). Platelet aggregation mediated by inflammation played a critical role in the development of coronary heart diseases (CHD). Our previous clinical researches showed that Th17 cells and their characteristic cytokine IL-17A were associated with the plaque destabilization in patients with acute coronary syndrome (ACS). The potent effect of IL17A on platelets-induced atherothrombosis remains unknown
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