Add time:08/23/2019         Source:sciencedirect.com

PC-3 cells, a metastatic human prostate adenocarcinoma line, caused dose-dependent platelet aggregation in heparinised human platelet-rich plasma (PRP). PC-3 tumour cell-induced platelet aggregation (TCIPA) was completely inhibited by hirudin (5 UIml) and limited by increasing concentrations of apyrase. This TCIPA was unaffected by cysteine proteinase inhibition with E-64 (10 μM), but was limited by cell pretreatment with phospholipase A2. PC-3 cell suspension caused marked, dosedependent decreases in plasma recalcification times using normal, Factor VHI-deficient and Factor IX-deficient, but not Factor Vll-deficient, human plasma. This effect was potentiated in cell lysates, but was inhibited in intact cells preincubated with sphingosine. Overall, these data suggest that PC-3 TCIPA arises from PC-3 tissue factor activity expression. trigramin (cas 111019-84-2) and rhodostomin, RGD-containing snake venom peptides which antagonise the binding of fibrinogen to platelet membrane glycoprotein Ilb-IIIa, prevented PC-3 TCIPA. Similarly, synthetic peptide GRGDS as well as monoclonal antibodies against platelet membrane glycoproteins Ilb-IIIa and Ib prevented PC-3 TCIPA, which was unaffected by control peptide GRGDS. On a molar basis, trigramin (IC50, 0.11 μM) and rhodostomin (IC50, 0.03 μM) were approximately 5000 and 18000 times, respectively, more potent than GRGDS (IC50, 0.56 mM).

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