Involvement of Cyclooxygenase, Phospholipase C and Map Kinase Pathways in Human Platelet Aggregation Mediated by the Synergistic Interaction of Platelet Activating Factor and Arachidonic Acid

2003 ◽  
Vol 6 (10) ◽  
pp. 918-924 ◽  
Author(s):  
S.A. Saeed ◽  
H. Rasheed . ◽  
S. Kumar . ◽  
T.M. Ali . ◽  
M.U. Butt . ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Map Kinase ◽  
Phospholipase C ◽  
Human Platelet ◽  
Platelet Activating Factor ◽  
Synergistic Interaction ◽  
Human Platelet Aggregation ◽  
Map Kinase Pathways

scholarly journals Phospholipase C-γ2 via p38 and ERK1/2 MAP kinase mediates diperoxovanadate-asparagine induced human platelet aggregation and sCD40L release

Redox Report ◽  
2013 ◽  
Vol 18 (5) ◽  
pp. 174-185 ◽  
Author(s):  
Ankita Misra ◽  
Smriti Srivastava ◽  
Seshadri Reddy Ankireddy ◽  
Nashreen S. Islam ◽  
Tulika Chandra ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Map Kinase ◽  
Phospholipase C ◽  
Human Platelet ◽  
Human Platelet Aggregation

Phospholipase C from Clostridium Perfringens Induces Human Platelet Aggregation in Plasma

1988 ◽  
Vol 59 (02) ◽  
pp. 236-239 ◽  
Author(s):  
Giovanna Barzaghi ◽  
Chiara Cerletti ◽  
Giovanni de Gaetano
Keyword(s):  
Platelet Aggregation ◽  
Receptor Antagonist ◽  
Phospholipase C ◽  
Clostridium Perfringens ◽  
Human Platelet ◽  
Ex Vivo ◽  
Platelet Rich Plasma ◽  
Platelet Activating Factor ◽  
Inhibitory Effect ◽  
Thromboxane Receptor Antagonist

SummaryWe studied the aggregating effect of different concentrations of phospholipase C (PLC) (extracted from Clostridium perfringens) on human platelet-rich plasma (PRP). PRP was preincubated with PLC for 3 min at 37° C and the platelet aggregation was followed for 10 min. The threshold aggregating concentration (TAG) of PLC was 3-4 U/ml.We also studied the potentiation of PLC with other stimuli on platelet aggregation. Potentiating stimuli, such as arachidonic acid (AA), ADP. Platelet Activating Factor (PAF) and U-46619 (a stable analogue of cyclic endoperoxides) were all used at subthreshold concentrations. We also studied the possible inhibitory effect of aspirin, apyrase, TMQ, a prostaglandin endoper- oxide/thromboxane receptor antagonist and BN-52021, a PAF receptor antagonist. Only aspirin and apyrase were able to reduce aggregation induced by PLC alone and PLC + AA and PLC + ADP respectively. TMQ and BN-52021 were inactive. In ex vivo experiments oral aspirin (500 mg) partially inhibited platelet aggregation induced by PLC alone, PLC + AA and PLC + ADP 2 and 24 h after administration. Aspirin 20 mg for 7 days also reduced aggregation induced by PLC + AA.

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