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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2008;28:1920.)
© 2008 American Heart Association, Inc.

Brief Reviews

Platelet Chemokines in Vascular Disease

Christian A. Gleissner; Philipp von Hundelshausen; Klaus Ley

From the Division of Inflammation Biology (C.A.G., K.L.), La Jolla Institute for Allergy and Immunology, Calif; and the Institute for Molecular Cardiovascular Research (IMCAR) (P.v.H.), University Hospital Aachen, Germany.

Correspondence to Klaus Ley, MD, Division of Inflammation Biology, La Jolla Institute for Allergy and Immunology, 9240 Athena Circle Drive, La Jolla, CA 92037. E-mail klaus{at}liai.org

Series Editor: Christian Weber
ATVB In Focus

Chemokines in Atherosclerosis, Thrombosis, and Vascular Biology

Platelets are a rich source of different chemokines and express chemokine receptors. CXCL4 is highly abundant in platelets and involved in promoting monocyte arrest from rolling and monocyte differentiation to macrophages. CXCL4 can also associate with CCL5 and amplify its effect on monocytes. The megakaryocyte CXCL7 gene product is proteolytically cleaved into the strong neutrophil chemoattractant, NAP-2, which has also been implicated in repair cell homing to vascular lesions. Platelet adhesion can induce release of CCL2 and CXCL8 from endothelial cells. Conversely, the chemokines CCL17, CCL22, and CXCL12 made by other cells amplify platelet activation. Platelet chemokines enhance recruitment of various hematopoietic cells to the vascular wall, fostering processes such as neointima formation, atherosclerosis, and thrombosis, but also vessel repair and regeneration after vascular injury.

Key Words: angiogenesis • atherosclerosis • platelets • thrombosis • chemokines

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