Platelet-derived chemokines in vascular biology

Abstract

SummaryUndoubtedly, platelets arek ey elements in the regulation of thrombosis andh aemostasis. Along with their primaryt ask to preventbloodloss from injuredvessels,platelets have emerged as regulators of av ariety of processes in the vasculature. Multiplec hallenges, from the contact and adhesion to subendothelialmatrix after injuryofthe vesselwall,tointeractions withbloodcells in inflammatory conditions,result in plateletactivation with concomitant shapec hangea nd releaseo fn umerous substances. Among these, chemokines have been found to modulate several processesi nt he vasculature, such as atherosclerosis and angiogenesis. In particular,the chemokinesc onKeywords Chemokines, plateletimmunology, atherosclerosis, angiogenesis and inhibitors nectivetissueactivating protein III (CTA P-III) and its precursors, or truncationp roducts (CXCL7),p lateletf actor 4, (PF4, CXCL4)a nd its variant PF4alt( CXCL4L1) or regulatedu pon activationand normal Tcellexpressedand secreted (RANTES, CCL5),h aveb een investigatedt horoughly. Defined common properties as their aptitude to bindglycosaminoglycans or their predisposition to associate and form homooligomersa re prerequisites fort heir role in the vasculaturea nd function in vivo. The current reviewsummarizes the developmentofthese single chemokines,and their cooperativee ffects that mayi np artb e dependentontheir physicalinteractions.

Hemopoietic Cell Expression of the Chemokine Decoy Receptor D6 Is Dynamic and Regulated by GATA1

“…Preliminary data suggest expression of D6 protein in human platelets and we are investigating potential roles for platelet D6 in the regulation of systemic chemokine levels and in vascular remodeling (50,51).…”

TNF-α alters the inflammatory secretion profile of human first trimester placenta

“…20,21 By complementary analysis, using the padlock probe approach, we detected CCL5 mRNA transcripts in the villous trophoblast compartment, suggesting that protein levels may probably have been too low to allow their detection by immunohistochemistry. In addition to platelets, also fibroblasts, mesangial cells, and epithelial cells express CCL5 on activation with TNF-α, 22 suggesting that villous trophoblast may contribute little amounts of CCL5 to the cocktail of released factors in response to inflammatory stimuli. Unlike villous trophoblast, which seems to only marginally express CCL5, trophoblast cell lines Swan 71 and HTR-8/SVneo clearly produce CCL5 (ref.…”

Distinct CCR2+Gr1+Cells Control Growth of theYersinia pestisΔyopMMutant in Liver and Spleen during Systemic Plague

“…This process activates integrins to cause arrest and then migration into tissues to inflammatory sites (8,31,39). Two prominent chemokines that selectively elicit migration of monocytes in many systems are CCL2/MCP-1 and CCL5/RANTES, which are produced by cytokine-stimulated platelets, cytokine-activated endothelial cells (ECs), stimulated mast cells, and stimulated resident macrophages (10,24,27,42,50,63) as well as stimulated PMNs (55). Additional chemokines not selective for migration of MOs can synergize with CCL2 (e.g., N-formyl-Met-Leu-Phe [fMLP], platelet-activating factor, and CXCL12/stromal cell-derived factor 1) (14).…”