OBJECTIVES: We sought to investigate the potential role of elevated levels of thrombopoietin (TPO) in platelet activation during unstable angina (UA). BACKGROUND: Thrombopoietin is a humoral growth factor that does not induce platelet aggregation per se, but primes platelet activation in response to several agonists. No data concerning its contribution to platelet function abnormalities described in patients with UA are available. METHODS: We studied 15 patients with UA and, as controls, 15 patients with stable angina (SA) and 15 healthy subjects. We measured TPO and C-reactive protein (CRP), as well as monocyte-platelet binding and the platelet expression of P-selectin and of the TPO receptor, c-Mpl. The priming activity of patient or control plasma on platelet aggregation and monocyte-platelet binding and the role of TPO in this effect also were studied. RESULTS: Patients with UA showed higher circulating TPO levels, as well as increased monocyte-platelet binding, platelet P-selectin expression, and CRP levels, than those with SA and healthy control subjects. The UA patients also showed reduced platelet expression of the TPO receptor, c-Mpl. In vitro, the plasma from UA patients, but not from SA patients or healthy controls, primed platelet aggregation and monocyte-platelet binding, which were both reduced when an inhibitor of TPO was used. CONCLUSIONS: Thrombopoietin may enhance platelet activation in the early phases of UA, potentially participating in the pathogenesis of acute coronary syndromes.
OBJECTIVES: We sought to investigate the potential role of elevated levels of thrombopoietin (TPO) in platelet activation during unstable angina (UA). BACKGROUND:Thrombopoietin is a humoral growth factor that does not induce platelet aggregation per se, but primes platelet activation in response to several agonists. No data concerning its contribution to platelet function abnormalities described in patients with UA are available. METHODS: We studied 15 patients with UA and, as controls, 15 patients with stable angina (SA) and 15 healthy subjects. We measured TPO and C-reactive protein (CRP), as well as monocyte-platelet binding and the platelet expression of P-selectin and of the TPO receptor, c-Mpl. The priming activity of patient or control plasma on platelet aggregation and monocyte-platelet binding and the role of TPO in this effect also were studied. RESULTS:Patients with UA showed higher circulating TPO levels, as well as increased monocyte-platelet binding, platelet P-selectin expression, and CRP levels, than those with SA and healthy control subjects. The UA patients also showed reduced platelet expression of the TPO receptor, c-Mpl. In vitro, the plasma from UA patients, but not from SA patients or healthy controls, primed platelet aggregation and monocyte-platelet binding, which were both reduced when an inhibitor of TPO was used. CONCLUSIONS:Thrombopoietin may enhance platelet activation in the early phases of UA, potentially participating in the pathogenesis of acute coronary syndromes.
Authors: Payam Fallahi; Richard Katz; Ian Toma; Ranyang Li; Jonathan Reiner; Kiersten VanHouten; Larry Carpio; Lorraine Marshall; Yi Lian; Sujata Bupp; Sidney W Fu; Frederick Rickles; David Leitenberg; Yinglei Lai; Babette B Weksler; Frederik Rebling; Zhaoqing Yang; Timothy A McCaffrey Journal: Gene Date: 2013-02-27 Impact factor: 3.688
Authors: Catherine M Hobbs; Harriet Manning; Cavan Bennett; Louella Vasquez; Sonia Severin; Lauren Brain; Alexandra Mazharian; Jose A Guerrero; Juan Li; Nicole Soranzo; Anthony R Green; Steve P Watson; Cedric Ghevaert Journal: Blood Date: 2013-10-01 Impact factor: 22.113
Authors: Christoph Tschuor; Lars M Asmis; Philipp M Lenzlinger; Martina Tanner; Luc Härter; Marius Keel; Reto Stocker; John F Stover Journal: Crit Care Date: 2008-06-18 Impact factor: 9.097