Platelets induce alterations of chemotactic and adhesive properties of endothelial cells mediated through an interleukin-1-dependent mechanism. Implications for atherogenesis

Gawaz, Meinrad; Brand, Korbinian; Dickfeld, Timm; Pogátsa-Murray, Gisela; Page, Sharon; Bogner, Christian; Koch, Werner; Schömig, Albert; Neumann, Franz Josef

doi:10.1016/s0021-9150(99)00241-5

Cited by 221 publications

(161 citation statements)

References 40 publications

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“…Thrombin in particular is a potent activator of platelets leading to increased P-selectin expression (10). Once activated, platelets may serve to potentiate the inflammatory response via the release of cytokines such as interleukin-1 (9), indeed platelet-derived interleukin-1 stimulates chemokine release and adhesion molecule expression in cultured endothelial cells (7).…”

Section: Discussionmentioning

confidence: 99%

Time-dependent platelet-vessel wall interactions induced by intestinal ischemia-reperfusion

Cooper

Chitman

Williams

et al. 2003

American Journal of Physiology-Gastrointestinal and Liver Physi

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roll and adhere in venules exposed to ischemia-reperfusion (I/R). This platelet-endothelial adhesion may influence leukocyte trafficking because platelet depletion decreases I/Rinduced leukocyte emigration. The objectives of this study were 1) to assess the time course of platelet adhesion in the small bowel after I/R and 2) to determine the roles of endothelial and/or platelet P-selectin and P-selectin glycoprotein ligand-1 (PSGL-1) in this adhesion. The adhesion of fluorescently labeled platelets was monitored by intravital microscopy in postcapillary venules exposed to 45 min of ischemia and up to 8 h of reperfusion. Peak platelet adhesion was observed at 4 h of reperfusion. To assess the contributions of platelet and endothelial cell P-selectin, platelets from Pselectin-deficient and wild-type mice were infused into wildtype and P-selectin-deficient mice, respectively. Platelets deficient in P-selectin exhibited low levels of adhesion comparable to that in sham-treated animals. In the absence of endothelial P-selectin, platelet adhesion was reduced by 65%. Treatment with a blocking antibody against PSGL-1 reduced adhesion by 57%. These results indicate that I/R induces a time-dependent platelet-endothelial adhesion response in postcapillary venules via a mechanism that involves PSGL-1 and both platelet and endothelial P-selectin, with platelet P-selectin playing a greater role.

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Section: Discussionmentioning

confidence: 99%

Time-dependent platelet-vessel wall interactions induced by intestinal ischemia-reperfusion

Cooper

Chitman

Williams

et al. 2003

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…4 All patients received ASA plus low-molecular-weight heparin. 5 There were 7 ASA + prasugrel recipients derived from the JUMBO trial and 124 ASA + clopidogrel recipients derived from a comparable historic cohort. 6 All patients received ASA.…”

Section: Platelets Inflammation and Antiinflammatory Drugs In Acs Anmentioning

confidence: 99%

“…During adhesion, platelets are activated and release potent inflammatory and mitogenic substances into the local microenvironment, thereby altering function of endothelial cells (4). These alterations support chemotaxis, adhesion and transmigration of monocytes to the site of inflammation (5). Platelets secrete or expose adhesion proteins, growth factors, chemokines, cytokine-like factors and coagulation factors (6,7).…”

mentioning

confidence: 99%

Platelets, inflammation and anti-inflammatory effects of antiplatelet drugs in ACS and CAD

Müller¹,

Chatterjee²,

Rath³

et al. 2015

Thromb Haemost

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SummaryPlatelets play a pivotal role in chronic inflammation leading to progression of atherosclerosis and acute coronary events. Recent discoveries on novel mechanisms and platelet-dependent inflammatory targets underpin the role of platelets to maintain a chronic inflammatory condition in cardiovascular disease. There is strong and clinically relevant crosslink between chronic inflammation and platelet activation. Antiplatelet therapy is a cornerstone in the prevention and treatment of acute cardiovascular events. The benefit of antiplatelet agents has mainly been attributed to their direct anti-aggregatory impact. Some anti-inflammatory off-target effects have also been described. However, it is unclear whether these effects are secondary due to inhibition of platelet activation or are caused by direct distinct mechanisms interfering with inflammatory pathways. This article will highlight novel platelet associated targets that contribute to inflammation in cardiovascular disease and elucidate mechanisms by which currently available antiplatelet agents evolve anti-inflammatory capacities, in particular by carving out the differential mechanisms directly or indirectly affecting platelet mediated inflammation. It will further illustrate the prognostic impact of antiplatelet therapies by reducing inflammatory marker release in recent cardiovascular trials.

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“…factor V, factor XI, PAI-1, plasminogen and protein S) (Gawaz et al, 2005). In vitro study revealed that activated platelets coincubated with cultured endothelial cells gave rise to a secretion of MCP-1 and surface expression of ICAM-1 and v 3 on endothelial cells, which is mediated by an IL-1-dependent mechanism (Gawaz et al, 2000). MCP-1 is an effectual chemotactic factor for monocytes and ICAM-1 is an adhesion molecule which advocates monocyte and neutrophil recruitment to endothelial cells.…”

Section: Tight Adhesion Of Platelet To Endothelial Cell Surfacementioning

confidence: 97%

Plaque, Platelets, and Plug – The Pathogenesis of Acute Coronary Syndrome

Hartopo¹,

Setianto²,

Hariawan³

et al. 2012

Acute Coronary Syndromes

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Platelets induce alterations of chemotactic and adhesive properties of endothelial cells mediated through an interleukin-1-dependent mechanism. Implications for atherogenesis

Cited by 221 publications

References 40 publications

Time-dependent platelet-vessel wall interactions induced by intestinal ischemia-reperfusion

Time-dependent platelet-vessel wall interactions induced by intestinal ischemia-reperfusion

Platelets, inflammation and anti-inflammatory effects of antiplatelet drugs in ACS and CAD

Plaque, Platelets, and Plug – The Pathogenesis of Acute Coronary Syndrome

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