TY - JOUR
T1 - Tumor necrosis factor-α as trigger of platelet activation in patients with heart failure
AU - Pignatelli, Pasquale
AU - De Biase, Luciano
AU - Lenti, Luisa
AU - Tocci, Giuliano
AU - Brunelli, Alessandra
AU - Cangemi, Roberto
AU - Riondino, Silvia
AU - Grego, Susanna
AU - Volpe, Massimo
AU - Violi, Francesco
PY - 2005/9/15
Y1 - 2005/9/15
N2 - The clinical history of patients with heart failure (HF) is complicated by arterial thromboembolism. Platelet activation is reported in this population, but the underlying mechanism has not been clarified. Forty-two patients with HF scored according to New York Heart Association (NYHA) classification had higher levels of collagen-induced platelet aggregation, platelet tumor necrosis factor-α (TNF-α) receptor expression, and serum thromboxane B 2 and higher circulating levels of TNF-α than 20 healthy subjects. Coincubation of platelets from HF patients with an inhibitor of TNF-α receptors significantly reduced collagen-induced platelet aggregation. In vitro study demonstrated that TNF-α amplified the platelet response to collagen; this effect was inhibited by TNF-α receptor antagonist and inhibitors of arachidonic acid metabolism. This study showed that TNF-α behaves as a trigger of platelet activation through stimulation of the arachidonic acid pathway.
AB - The clinical history of patients with heart failure (HF) is complicated by arterial thromboembolism. Platelet activation is reported in this population, but the underlying mechanism has not been clarified. Forty-two patients with HF scored according to New York Heart Association (NYHA) classification had higher levels of collagen-induced platelet aggregation, platelet tumor necrosis factor-α (TNF-α) receptor expression, and serum thromboxane B 2 and higher circulating levels of TNF-α than 20 healthy subjects. Coincubation of platelets from HF patients with an inhibitor of TNF-α receptors significantly reduced collagen-induced platelet aggregation. In vitro study demonstrated that TNF-α amplified the platelet response to collagen; this effect was inhibited by TNF-α receptor antagonist and inhibitors of arachidonic acid metabolism. This study showed that TNF-α behaves as a trigger of platelet activation through stimulation of the arachidonic acid pathway.
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U2 - 10.1182/blood-2005-03-1247
DO - 10.1182/blood-2005-03-1247
M3 - Article
C2 - 15956282
AN - SCOPUS:24744432090
VL - 106
SP - 1992
EP - 1994
JO - Blood
JF - Blood
SN - 0006-4971
IS - 6
ER -