PGE1 and PGE2 modify platelet function through different prostanoid receptors

P2Y12and EP3 antagonists promote the inhibitory effects of natural modulators of platelet aggregation that act via cAMP

“…The overall effect is inhibition of platelet aggregation because the effect at IP outweighs the effect at EP3. Nevertheless, as demonstrated here and previously [25], the EP3 receptor antagonist DG-041 enhances the overall inhibitory effect of PGE 1 on platelet aggregation. The new information provided here is that the combination of DG-041 and a P2Y 12 antagonist which together block the effects of both PGE 1 and ADP at their G i -linked receptors, produces even further inhibition of platelet function.…”

“…Samples were then frozen and stored at À20 C prior to assay. The amounts of the phosphorylated form of VASP (VASP-P) present in the lysates were measured using a flow cytometric bead assay which has been described previously [25,[27][28][29]. Briefly, platelet lysates (25 ml) were incubated with APC-fluorescent beads (Becton Dickinson) (25 ml) coated with a monoclonal antibody to VASP (mAb IE273 anti-VASP conjugated using the Functional Bead Conjugation Buffer Set).…”

“…They have the ability to both promote platelet function through interaction with EP3 receptors, and to inhibit platelet function through interaction with receptors linked to G s , with the overall effect being the balance between these opposing actions. PGE 1 inhibits platelet function acting via G slinked IP receptors [25] and PGE 2 inhibits platelet function mainly via EP4 receptors [25][26][27][28].…”

Characterization of an arachidonic acid-deficient (Fads1 knockout) mouse model

“…5 ). Interestingly, 1-series derived prostaglandins, e.g., PGE 1 , interact with discrete receptors compared with PGE 2 ( 30,31 ). This is noteworthy, because PGE 1 is capable of inhibiting colon cancer cell proliferation ( 32,33 ) as opposed to PGE 2 , which promotes growth ( 1,34 ).…”

Enhanced Ca2+ response and stimulation of prostaglandin release by the bradykinin B2 receptor in human retinal pigment epithelial cells primed with proinflammatory cytokines

“…Similarly to what observed for BK-evoked intracellular Ca 2+ elevation, synergistic stimulation of prostaglandin formation by BK and cytokines was exclusively due to activation of the kinin B 2 receptor. The fact that BK and cytokines induced both PGE 1 and PGE 2 production is of particular importance since PGE 1 might exert a distinct action profile compared with that of PGE 2 as it had high affinity for prostaglandin IP receptor, whereas PGE 2 had a high affinity for prostaglandin FP in addition to EP receptors [41,42]. In particular, PGE 1 displayed a strong angiogenic response at lower dose as compared to PGE 2 in the rabbit corneal test [43].…”