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Review
. 2008 Nov;28(11):1920-7.
doi: 10.1161/ATVBAHA.108.169417. Epub 2008 Aug 21.

Platelet chemokines in vascular disease

Christian A Gleissner  1 , Philipp von Hundelshausen, Klaus Ley
Affiliations
Review

Platelet chemokines in vascular disease

Christian A Gleissner et al. Arterioscler Thromb Vasc Biol. 2008 Nov.

Abstract

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.

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Figures

Figure 1
Figure 1
Amino acid sequences of the differentially truncated peptide forms of CXCL7. Starting with pro-PBP in megakaryocytes, sequential proteolytic modification (bold arrows) generates different CXCL7 peptides with different biological functions which are indicated by small arrows. NAP-2 is the chemotactically most active form of CXCL7. Further truncation including the ELR domain (bold) results in loss of activity. The inserts depicts the tertiary structure of pro-PBP as given by protein database (PDB).
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