2001
DOI: 10.1097/00000542-200101000-00025
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Leukocytes Can Enhance Platelet-mediated Aggregation and Thromboxane Release via  Interaction of P-selectin Glycoprotein Ligand 1 with P-selectin

Abstract: Leukocytes can enhance platelet agonist--induced aggregation and thromboxane release in whole blood and platelet-rich plasma under shear conditions in vitro. Interaction of platelet P-selectin with leukocyte PSGL1 contributes substantially to these effects.

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Cited by 67 publications
(49 citation statements)
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“…8,9 Shear stress can also cause leukocyte activation in vitro, 8,9 which can in turn promote platelet activation. 41 However, it is unclear whether platelet or leukocyte activation is separately or sequentially up-regulated across coronary stenoses. Results from the in vitro arm of this study show that CD62P blockade completely suppressed shear-induced platelet-monocyte aggregation with no effect on shear-induced monocyte CD11b expression (Figure 10).…”
Section: Discussionmentioning
confidence: 99%
“…8,9 Shear stress can also cause leukocyte activation in vitro, 8,9 which can in turn promote platelet activation. 41 However, it is unclear whether platelet or leukocyte activation is separately or sequentially up-regulated across coronary stenoses. Results from the in vitro arm of this study show that CD62P blockade completely suppressed shear-induced platelet-monocyte aggregation with no effect on shear-induced monocyte CD11b expression (Figure 10).…”
Section: Discussionmentioning
confidence: 99%
“…According to Faraday, et al this effect can be explained by the interaction of platelet P-selectin with leukocyte P-selectin glycoprotein ligand-1 leading to an enhanced platelet agonist-induced aggregation and thromboxane release [22].…”
Section: Discussionmentioning
confidence: 99%
“…A variety of chemokines and leukocyte interactions via surface receptors have been reported to modulate platelet function and contribute to activation of platelets. [25][26][27] Theoretically, such a marked systemic inflammatory activity might be further increased by bile duct stenosis, malignancy, and radiotherapy. However, there is no convincing evidence that these mechanisms really have a clinical impact post transplant.…”
Section: See Article On Page 1372mentioning
confidence: 99%