Abstract
Platelets are small anucleated cells present only in mammals. Platelets mediate intravascular hemostatic balance, prevent interstitial bleeding, and have a major role in thrombosis. Activation of platelet purinergic receptors is instrumental in initiation of hemostasis and formation of the hemostatic plug, although this activation process becomes problematic in pathological settings of thrombosis. This review briefly outlines the roles and function of currently known platelet purinergic receptors (P1 and P2) in the setting of hemostasis and thrombosis. Additionally, we discuss recent novel studies on purinergic receptor distribution according to heterogeneous platelet size, and the possible implication of this distribution on hemostatic function.
Highlights
Adenine nucleosides and nucleotides accumulate in the circulation under various pathological conditions and can initiate and mediate the response to cell damage, hypoxia, and inflammation (Koupenova and Ravid, 2013)
One of the mechanisms by which cyclic AMP (cAMP) reduces platelet aggregation involves activation of protein kinase A (PKA) which leads to the phosphorylation and inhibition of inositol 1,4,5triphosphate (IP3) receptor-mediated increase of calcium from the dense tubular system; reduced levels of cAMP have the opposite effect on IP3 and increase intracellular calcium (Quinton and Dean, 1992; Tertyshnikova and Fein, 1998)
The platelet mRNA profile may have a broader impact on overall platelet function, and proposes an explanation of previously identified functional differences between small and large platelets, with increased mean platelet volume being historically associated with increased hemostatic potential
Summary
Adenine nucleosides and nucleotides accumulate in the circulation under various pathological conditions and can initiate and mediate the response to cell damage, hypoxia, and inflammation (Koupenova and Ravid, 2013). The distinct distribution of P-selectin expressing platelets in the core vs P-selectin-negative platelets in the shell suggests a possibility for a specific distribution of different platelet subpopulations throughout the hemostatic plug, according to their function in the interaction with either damaged endothelium or circulating leukocytes.
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