Platelet P-selectin plays an important role in arterial thrombogenesis by forming large stable platelet-leukocyte aggregates.

Objectives: We investigated the role of P-selectin in arterial thrombogenesis by forming large stable platelet-leukocyte aggregates.

Background: Plaque rupture followed by thrombus formation is a fundamental pathophysiology of acute coronary syndromes. Although the adhesive interaction between platelets and leukocytes via P-selectin is known to mediate platelet-rich thrombi, the true function of P-selectin in thrombus formation in vivo is unknown.

HMG-CoA reductase inhibitor protects against in vivo arterial thrombosis by augmenting platelet-derived nitric oxide release in rats.

Acute coronary syndromes are caused by platelet-mediated thrombosis following rupture of a plaque. HMG-CoA reductase inhibitors (statins) reduce the incidence of events early after acute coronary syndromes, which are independent of its cholesterol-lowering effect. Accordingly, we investigated whether statins inhibit platelet-mediated arterial thrombus formation in vivo and, if so, the underlying mechanisms.

Only two-week smoking cessation improves platelet aggregability and intraplatelet redox imbalance of long-term smokers.

Objectives: We investigated whether and how soon smoking cessation ameliorates the smoking-induced intracellular oxidative stress and platelet aggregability in long-term smokers.

Background: Smoking is a major risk factor of atherothrombosis. Smoking cessation reduces cardiac events.

Inhibition of platelet adherence to mononuclear cells by alpha-tocopherol: role of P-selectin.

Background: Platelet-leukocyte interaction is an early important event for thrombogenesis, and this process is mainly mediated by P-selectin on platelets. Although alpha-tocopherol has been shown to inhibit thrombotic disorders, the effect of alpha-tocopherol on platelet P-selectin expression and platelet-leukocyte interaction is little known.

Methods And Results: We examined whether alpha-tocopherol inhibited human platelet P-selectin expression and platelet-leukocyte interaction.

Vitamin E inhibits lysophosphatidylcholine-induced endothelial dysfunction and platelet activation.

Lysophosphatidylcholine (LPC), a lysolipid contained in oxidized low-density lipoprotein, is an atherogenic molecule that induces endothelial dysfunction and platelet activation and inhibits angiogenesis. Although studies showed that vitamin E has antiatherogenic properties, the effects of vitamin E on LPC-induced endothelial dysfunction and platelet activation are little known. We examined whether vitamin E has protecting actions against LPC-induced alterations of endothelial and platelet functions.

Coexistence of impairment of endothelium-derived nitric oxide and platelet-derived nitric oxide in patients with coronary risk factors.

Impairment of endothelium-derived nitric oxide (EDNO) has been demonstrated in patients with coronary risk factors in some studies, as well as impaired platelet-derived nitric oxide (PDNO) in other studies. However, no study has examined whether these impairments coexist. In 24 patients with coronary risk factors, femoral vascular endothelial function was assessed with acetylcholine (ACh: 50, 100, 200 and 400 microg/min) and endothelium-independent vascular function with nitroglycerin (NTG; 50, 100, 200 microg/min) using a Doppler flow-wire technique, as well as ADP (5 micromol/L)-induced PDNO release with an NO-specific electrode.