122 (2019) 154157

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Cytokine

journal homepage: www.elsevier.com/locate/cytokine

Platelet-derived in and T ⁎ Constantinos Bakogiannisa, Marco Sachseb,c,d, Kimon Stamatelopoulose, Konstantinos Stellosb,c,d, a 3rd Department of Cardiology, Ippokrateio Hospital, Aristotle University of Thessaloniki, Thessaloniki, Greece b Institute of Cardiovascular Regeneration, Centre of Molecular Medicine, Goethe University Frankfurt, Frankfurt/Main, Germany c German Center of Cardiovascular Research (DZHK), Frankfurt/Main, Germany d Department of Cardiology, Goethe University Frankfurt, Frankfurt/Main, Germany e Department of Clinical Therapeutics, Alexandra Hospital, National and Kapodistrian University of Athens, Athens, Greece

ARTICLE INFO ABSTRACT

Keywords: Platelets are inflammatory anuclear cells with a well-established role in the development and manifestation of Atherosclerosis atherosclerosis. Activated platelets secrete a plethora of chemokines including CXCL4 or (PF4), Platelets CCL5, CXCL12 or stromal cell derived factor-1α (SDF-1α), CXCL16 and others, which initiate or promote local Inflammation inflammatory processes at sites of vascular injury. These processes are mainly mediated by the recruitment of Chemokines circulating haematopoietic stem cells, neutrophils, or lymphocytes on vascular wall. Under acute Coronary artery disease ischemic conditions platelet-derived chemokines may promote the mobilization of bone marrow-derived pro- genitor cells and their homing at lesion sites. This review focuses on the role of platelet-derived chemokines in inflammation and atherosclerosis. Further, we discuss the clinical value of plasma levels of chemokines inthe prognosis of atherosclerotic heart disease.

1. Introduction receptor interact with circulating activated platelets, even under high shear stress conditions, leading to platelet adhesion to vascular wall Atherosclerosis represents a complex immune response to oxidized [4–7]. Upon adhesion, platelets release a plethora of pro-inflammatory low-density lipoprotein or other unknown antigens facilitated by in- chemokines, which attract circulating leukocytes favoring the recruit- terplay between various cell populations in atheromatous plaque. This ment of the latter to vascular wall [8]. Moreover, inflammatory med- cellular interaction on vascular wall is fired or enhanced by a plethora iators released from activated platelets promote vascular inflammation of chemokines, which are secreted or expressed in the surface of all at lesion sites. Specifically, the CCL5 (also known as vascular and blood cells including platelets [1]. A constantly growing RANTES) and the dyad CD40-CD40L promote the recruitment of other number of data are indicating platelets as an actively involved cell platelets and inflammatory cells, thus contributing to the progression of population in atherosclerosis, as well as a crucial crosslink between atherosclerosis [3,8,9]. In addition, platelet released platelet factor-4 inflammation and thrombosis [2]. Though platelets do not adhere to the (PF4; also known as CXCL4) or stromal cell-derived factor-1 (SDF-1) vascular endothelium under normal (physiological) conditions, en- favor the uptake of oxidized LDL from promoting the dothelial cell activation towards a pro-inflammatory phenotype or formation of foam cells and contributing to the development of the lipid disruption of the endothelial layer, leads to platelet adhesion on vas- core of atherosclerotic plaques [10–12]. cular wall. Subsequently, platelet activation induces the re