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ADP receptor antagonists inhibit platelet aggregation induced by the chemokines SDF‐1, MDC and TARC
Author(s) -
Suttitanamongkol S,
Gear A.R.L
Publication year - 2001
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(00)02413-3
Subject(s) - pertussis toxin , chemokine , chemistry , receptor , platelet , stimulation , chemokine receptor , g protein , pharmacology , microbiology and biotechnology , biochemistry , immunology , biology , endocrinology
The ability of the chemokines SDF‐1, MDC and TARC to induce platelet aggregation depends strongly on low levels of ADP. The ADP receptors involved have now been characterized using the P2Y 1 and P2T AC receptor antagonists, A2P5P and AR‐C69931MX. Stimulation of aggregation by the chemokines at 10 s was not blocked by AR‐C69931MX, but was strongly inhibited by A2P5P. Pertussis toxin abolished the chemokine‐stimulated aggregation. We conclude that the P2Y 1 ADP receptor plays a critical role in the initial phases of SDF‐1‐, MDC‐ and TARC‐induced platelet aggregation, which involve a pertussis toxin‐sensitive G protein.