High impact information on Butaprost

• [(3)H]PGE(2) binding to cell membranes identified a high-affinity binding site that was competitively inhibited by M&B28767 (EP(3)/EP(4)) > 1-OH-PGE(1) (EP(4)) > sulprostone (EP(3)/EP(1)) > butaprost (EP(2)) [1].
• Comparison of prostaglandin F2alpha, bimatoprost (prostamide), and butaprost (EP2 agonist) on Cyr61 and connective tissue growth factor gene expression [2].
• In contrast, the EP2 receptor agonist butaprost, not the E1/E3 receptor agonist sulprostone, stimulated the expression of Cx43 and gap junction function [3].
• The inhibitory effects of ONO-604 on TNF-alpha and IL-12 production were equipotent with PGE(2) at any time point, but the inhibitory effects of butaprost were only seen from 14 h after stimulation [4].
• PGE(2) or dibutyryl cAMP alone, but not butaprost, reduced EP(4) expression, and indomethacin reversed the LPS-induced down-regulation of EP(4), indicating that the down-regulation of EP(4) is mediated by LPS-induced PG synthesis and EP(4) activation [4].

Biological context of Butaprost

• Moreover, PGE2 and Butaprost treatment elicited in orbital cultures a massive increase in endogenous cAMP production while analogues not affecting cell shape failed to influence cyclic nucleotide generation [5].
• PGE(2) and butaprost phosphorylated Bad and KT-5720 blocked phosphorylation [6].
• The membrane potential hyperpolarized significantly after PGE(2), butaprost, AE1-329 and AE1-259 and outward current was augmented in a PKA-dependent fashion [7].
• Using selective agonists, we found that butaprost, an EP(2)R agonist, and PGE(1) alcohol, an EP(2)R and EP(2)R/EP(4)R agonist, inhibited major histocompatibility complex class II expression and enhanced interleukin-10 production from DC [8].
• Northern Blot analysis revealed that PGF(2alpha)- and Butaprost-induced upregulation of Nur77 expression are dose- and time-dependent [9].

Anatomical context of Butaprost

• The EP2 receptor agonist butaprost did not change membrane voltage of podocytes [10].
• The order of potency of PGs for competition with binding of [3H]PGE2 to membranes prepared from COS-7 cells transfected with Hup-4 was PGE2 > or = PGE1 > 16,16-dimethyl-PGE2 > or = 11-deoxy-PGE1 > butaprost > AH13205 > 19(R)-OH-PGE2 [11].
• RESULTS: Butaprost had no significant effect on aqueous humor flow or total outflow facility in ocular normotensive monkeys [12].
• Further, migration in fibroblasts deficient for the EP2 receptor cannot be inhibited by PGE(2) or butaprost, confirming the central role of EP2 in mediating these effects [13].
• RO1138452 did not block relaxation of guinea-pig trachea induced by the EP(2)-selective agonist butaprost [14].

Associations of Butaprost with other chemical compounds

• Quantitative RT-PCR indicated that the mRNA for the murine EP4 receptor, the butaprost-insensitive PGE2 receptor that couples to Gs, increases 1.5-3-fold in response to serum (NIH 3T3) or LPS (RAW 264.7) with a time course approximating the induction of PGHS-2 expression [15].
• Furthermore, the EP1 receptor-selective antagonists AH 6809 and SC19220 were more potent than the EP2 receptor-selective agonist butaprost in these competition binding assays [16].
• PGE2 and the prostaglandin agonists, but not the IP receptor agonist iloprost and the EP2 receptor agonist butaprost, induced a time- and concentration-dependent cAMP accumulation in podocytes [10].
• Effects on ocular morphology were studied after tissue fixation with transcardial perfusion by paraformaldehyde and immersion fixation of the globe, in animals subjected to long-term treatment with butaprost [12].
• Only PGE(2) and PGE1 alcohol completely abolished CD36 induction by aspirin, whereas butaprost strongly reduced it [17].

Gene context of Butaprost

• We now report that both PGE(2) and butaprost increase PTEN phosphatase activity, without a concomitant increase in PTEN protein levels [13].
• Induction of COX-2 expression was also elicited by butaprost (EP(2) receptor agonist) and 11-deoxy PGE(1) (EP(2)/EP(4) receptor agonist), but not by EP(1)/EP(3) receptor agonists (17-phenyl-omega-trinor PGE(2), sulprostone) [18].
• Butaprost, a selective EP2 agonist, and ONO-AE1-329, a selective EP4 agonist, significantly inhibited IL-1alpha-induced MMP-3 production, although butaprost was less potent than ONO-AE-1-329 [19].
• The EP4 receptor-specific agonist, 11-deoxy-PGE1, induced a time-dependent phosphorylation of protein kinase C and extracellular signal-regulated kinase (ERK) 1/2 in serum-depleted (0.1%) VSMCs, whereas the EP2 receptor agonist, butaprost, was without effect [20].
• The EP1 selective agonist iloprost and the EP2 selective agonist butaprost minimally stimulated RANKL [21].

Analytical, diagnostic and therapeutic context of Butaprost

• The effects of butaprost on aqueous humor flow were determined by fluorophotometry [12].
• The eyes of separate groups of EP(1) receptor knockout and wild type mice were: 1) treated topically with prostaglandin E(2) (PGE(2)) or the EP(2) receptor selective agonist, butaprost; 2) given intravitreal injection of LPS; or 3) paracentesis performed [22].

References