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Lievens, D., Zernecke, A., Seijkens, T., Soehnlein, O., Beckers, L., Munnix, I.C., Wijnands, E., Goossens, P., van Kruchten, R., Thevissen, L., Boon, L., Flavell, R.A., Noelle, R.J., Gerdes, N., Biessen, E.A., Daemen, M.J., Heemskerk, J.W., Weber, C. and Lutgens, E. (2010) Platelet CD40L Mediates Thrombotic and Inflammatory Processes in Atherosclerosis. Blood, 116, 4317-4327.
http://dx.doi.org/10.1182/blood-2010-01-261206

has been cited by the following article:

• TITLE: In Vitro Effect of Soy Isoflavone and Equol on Soluble CD40L Release Stimulated by Ristocetin in Platelets from Postmenopause Women

  AUTHORS: Natalia Gonzalez, Argelia Garrido, Ingrid Acevedo, Luis Valladares

  KEYWORDS: Platelet, sCD40L, Phyoestrogen, Isoflavone, Equol

  JOURNAL NAME: Journal of Biomedical Science and Engineering, Vol.8 No.1, January 16, 2015

  ABSTRACT: The inhibition of specific flavonoid on the in vitro platelet aggregation induced by collagen, arachidonic acid and thromboxane A2 (TxA2) agonist, seems to be related mostly to their ability to compete for binding to the TxA2 receptor (TP). The aim of this study was to analyze the effect of soy isoflavone and equol in terms of inhibiting the platelet aggregation and sCD40L release stimulated by ristocetin, an in vitro-activator of glycoprotein Ib/IX/V, in platelets from postmenopausal women. When platelets were stimulated by 0.75 mg/ml ristocetin, equol (10 μM) exhibited a greater inhibitory activity on platelet aggregation (~68%) than genistein or daidzein. The effect of equol was dependent on the concentration of platelet aggregation agonist. In the presence of ristocetin (0.75 mg/ml, 1.125 mg/ml and 1.5 mg/ml), the inhibitory effect of 10 μM equol was 68% ± 5%, 54% ± 4% and 31% ± 5%, respectively. Equol (10 μM) was a potent inhibitor (~35%) of sCD40L release when stimulated with 1.5 mg/ml ristocetin. However, no significant differences were noted in platelets incubated in the presence of genistein or daidzein and stimulated by ristocetin. On the other hand, SQ29548, a high TP antagonist, also inhibited the sCD40L release stimulated by ristocetin. Finally, 10 μM of genistein, daidzein or equol did not significantly affect the thromboxane B2 production when platelets were incubated with 1.5 mg/ml ristocetin. The relevance of this study was to find that equol exhibits a potent activity by inhibiting ristocetin-induced sCD40L release, suggesting that soy isoflavone has important biological effects on the hemostatic system. However, clinical trials will be necessary to assess the effect of equol on platelet and their impact on inflammatory markers.