High impact information on Doproston

• MATERIALS AND METHODS: A bone marrow culture system and bone marrow macrophages were used to examine the effects of SC-19220 on PGE2-, 11-deoxy-PGE1-, and RANKL-induced osteoclastogenesis [1].
• Alkaline phosphatase-positive nodule formation in the absence or presence of XT-611 was inhibited by an antagonist of EP4 receptor, AH23848B, and synergistically potentiated by 11-deoxy-PGE1, but it was not influenced by other EP antagonists and agonists examined [2].
• RESULTS: PGE2 and cyclic AMP inhibited spontaneous eosinophil apoptosis at both 16 and 40 hours as did the PGEP2 receptor agonist, 11-deoxy PGE1, at 40 hours, but these effects were not inhibited by a protein kinase A antagonist [3].
• In contrast, 11-deoxy-PGE1 failed to inhibit the ERK activity in SHRSP-MCs [4].
• Butaprost, an EP2-selective agonist, showed effects similar to those of 11-deoxy-PGE1 only at confluency [5].

Biological context of Doproston

• The EP4 agonist, 11-deoxy-PGE1, inhibited sulprostone-induced phosphorylation of ERK in WKY-MCs [4].
• Incomplete displacement of labeled 3H-PGE2 from its binding sites by the EP2 selective agonist 11-deoxy PGE1 suggests the presence of additional EP or non-EP binding sites [6].

Anatomical context of Doproston

• 4. Oocytes with good responsiveness to PGE also produced K+ currents to PGA1, PGA2, PGB1, 11-deoxy-PGE1 and 11-beta-PGE2, whereas PGF2 alpha, PGI2, PGD2 and 8-iso-PGE1 generally failed to elicit membrane currents [7].
• METHODS: Human ciliary smooth muscle cells were grown to confluence in monolayer cell cultures and then treated with PGF2 alpha, 17-phenyltrinor-PGF2 alpha, or 11-deoxy-PGE1 [8].
• In actively growing, non-confluent primary keratinocyte cultures, the EP2 and EP4 selective agonists, 11-deoxy PGE1 and 1-OH PGE1, caused complete reversal of indomethacin-induced growth inhibition [9].

Associations of Doproston with other chemical compounds

• Indomethacin had little effect on the response to PGE2, or the relatively non-selective EP receptor agonists 11-deoxy PGE1 and misoprostol, but blocked the effects of PGF2alpha and the F receptor agonist fluprostenol, indicating an indirect action via release of other prostaglandins [10].

Gene context of Doproston

• 11-Deoxy-PGE1, and EP2 and EP4 agonist, decreased DNA synthesis and increased alkaline phosphatase activity at both stages [5].
• Northern blot analyses show that 11-deoxy PGE1, an EP2/EP4 agonist, emulates the action of PGE2 [11].
• An EP2/EP4 agonist, 11-deoxy-PGE1, attenuated IFN-gamma-elicited ICAM-1 expression in a concentration-dependent manner [12].
• A specific EP4 antagonist, AH-23848B, showed no effect on inhibition of IFN-gamma-elicited ICAM-1 expression by PGE2 and 11-deoxy-PGE1 [12].
• Another and more differentiated osteoblastic marker, osteocalcin production, was detectable and was stimulated by 11-deoxy-PGE1 only 5 days after confluency [5].

References