Akademik Veri Yönetim Sistemi
TBS International Biochemistry Congress 2021-32nd National Biochemistry Congress, Gaziantep, Türkiye, 27 - 30 Ekim 2021, ss.61, (Özet Bildiri)
BACKGROUND AND AIM: P2Y12 receptor is stimulated by ADP and, platelets
are activated. This receptor has been shown to be inhibited by UTP. It has been
shown that UDP plays a role in platelet-leukocyte interaction via P2Y14 receptor
and has no effect on hemostasis. Effects of uridine nucleotides on hemostasis via
different purinergic receptors are not yet fully known.
METHODS: Blood samples from volunteers, as whole blood and platelet-rich
plasma (PRP), were used in experiments to investigate the role of UDP and UTP
in hemostasis. Platelet aggregation tests showed that UTP and UDP inhibited
ADP-induced platelet aggregation.
RESULTS: Thromboelastogram experiments were performed in whole
blood. While UTP showed a hypocoagulant effect as if supporting the
finding in aggregation, UDP showed a hypercoagulant effect on the contrary.
In thromboelastogram experiments with PRP, both UTP and UDP showed
hypocoagulant effect.
CONCLUSIONS: Based on UTP antagonism of P2Y12 receptors, both
its inhibition in aggregometry and thromboelastogram can be understood.
Inhibition of ADP-induced platelet aggregation by UDP in the aggregometer
can be considered through P2Y12 antagonism. Experiments with PRP in the
thromboelastogram support this finding. However, hypercoagulant effect of
UDP in whole blood on thromboelastogram can be explained through P2Y14
receptors. It is known that UDP also stimulates P2Y6 and P2Y14 receptors
on leukocytes. Stimulation of these receptors increases leukocyte chemotaxis
and NET formation. The occurrence of platelet-leukocyte interaction by
activating P2Y14 receptors with UDP may explain the hypercoagulant effect.
UDP exerts its hypercoagulant effect in whole blood through the platelet leukocyte interaction and may be important in prothrombotic processes.