Purification and Characterization of Prostaglandin H Synthase-2 from Sheep Placental Cotyledons

Johnson, Jack; Wimsatt, Jeffrey; Buckel, Scott D.; Dyer, Richard D.; Maddipati, Krishna Rao

doi:10.1006/abbi.1995.9934

Cited by 110 publications

(89 citation statements)

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“…Celecoxib showed the strongest effect on cell proliferation, and this was correlated with the lower IC 50 reported for this compound toward COX-2 (0.04 μM vs. 1.27 μM for nimesulide and 1.77 μM for NS-398). 57 In addition, similar results have been obtained with hematological malignant cell lines such as Raji, BjAB (Epstein-Barr virus negative cell line) and BL41 (Burkitt's lymphoma). 58 In these cell lines, celecoxib was also able to inhibit cell proliferation.…”

Section: Cox-2 Inhibitors Impair C-myc Expressionsupporting

confidence: 63%

Cox-2 inhibitors induce early c-Myc downregulation and lead to expression of differentiation markers in leukemia cells

Sobolewski

Cerella²,

Dicato³

et al. 2011

Cell Cycle

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Section: Cox-2 Inhibitors Impair C-myc Expressionsupporting

confidence: 63%

Cox-2 inhibitors induce early c-Myc downregulation and lead to expression of differentiation markers in leukemia cells

Sobolewski

Cerella²,

Dicato³

et al. 2011

Cell Cycle

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“…18,25) The present results showed that the IC 50 value of Asp for COX-1 (0.56±0.11 mM) or COX-2 (1.36± 0.14 mM) is similar to the reported results (one sample Student t-test, p＞0.05). 22) The selective inhibition index of Asp for COX-2 is 0.42±0.12 (＜1), which supports the fact that Asp is a nonselective inhibitor of COX. 22) The results also showed that Cu-Asp inhibited COX-1 and COX-2 in a concentration-dependent manner with an IC 50 value of 1.03±0.20 mM for COX-1 and 0.32±0.05 mM for COX-2.…”

Section: Discussionsupporting

confidence: 56%

“…Asp is a well-known nonselective COX inhibitor, and the IC 50 value for COX-1 and COX-2 is 0.75 and 1.25 mM in ovine cells, respectively. 22) Our early study and other studies found that Cu-Asp had an more powerful antiin‰ammatory eŠect than Asp with fewer adverse eŠects. 5,6,23) Since Cu-Asp is a derivate from Asp, the mechanism of action of CuAsp may be similar to that of Asp.…”

Section: Discussionmentioning

confidence: 71%

Copper-Aspirin Complex Inhibits Cyclooxygenase-2 More Selectively than Aspirin

Peng

Zheng

et al. 2007

YAKUGAKU ZASSHI

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A: Cu-Asp tetrakis-mu-acetylsalicylato-dicopper (II) MW: 844 B: Aspirin MW: 180 1869 YAKUGAKU ZASSHI 127(11) 1869-1875 (2007) The antiin‰ammatory eŠects of the copper-aspirin complex (Cu-Asp) were more potent than that of Asp in rats or mice with fewer classic adverse eŠects. The aim of this study was to determine the cause by evaluating Cu-Asp selective inhibition on cyclooxygenases (COX). COX-1 inhibition was evaluated based on 6-keto-prostaglandin F 1a (6-keto-PGF 1a ) in an endothelial cell model, and COX-2 inhibition was based on prostaglandin E 2 (PGE 2 ) in a macrophage model. Radioimmunoassay (RIA) was applied to determine 6-keto-PGF 1a in resting human umbilical vein endothelial cell line (ECV304), and PGE 2 in activated macrophages. The results showed that the inhibition of 6-keto-PGF 1a yield by Cu-Asp (3 to 0.01 mM) was markedly weaker than that by aspirin (Asp); while the inhibition of PGE 2 yield by Cu-Asp (10 to 0.1 mM) was signiˆcantly stronger than that by Asp. Based on the inhibition on 6-keto-PGF 1a and PGE 2 , the medium inhibitory concentration (IC 50 ) of Cu-Asp on COX-1 and on COX-2 was 1.03±0.15 mM, and 0.32±0.04 mM, respectively. The selective inhibition index on COX-2, IC 50 (COX-1)/IC 50 (COX-2), of CuAsp was 3.33±0.89, while that of Asp was 0.42±0.12. The results suggest that, unlike Asp, Cu-Asp is a relatively selective inhibitor of COX-2 in the present models; the selectivity of Cu-Asp is about seven-fold greater than that of Asp.

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“…14 C]5,6-EET by cyclooxygenase was examined by incubating 2.6 or 14.2 g of purified COX-1 (from ram seminal vesicles; Cayman Chemical) or COX-2 (obtained from sheep placenta; Cayman Chemical) with 250 nmol of [ 14 C]5,6-EET (ϳ30 nCi) at 37°C in 100 mM Tris-HCl buffer solution, pH 8.0, containing 2 mM phenol and 1 M hematin (Smith and Marnett, 1991;Johnson et al, 1995). In some incubations, selective inhibition of COX isoforms was examined by the addition of either SC-560 or DUP-697 to the reaction mixtures 30 min before the addition of jpet.aspetjournals.org at 2 min by the addition of ice-cold acidified acetonitrile.…”

Section: Metabolism Of [ 14 C]56-eet By Cox-1 and Cox-2 Metabolism mentioning

confidence: 99%

Cyclooxygenase (COX)-1 and COX-2 Participate in 5,6-Epoxyeicosatrienoic Acid-Induced Contraction of Rabbit Intralobar Pulmonary Arteries

Moreland¹,

Procknow²,

Sprague³

et al. 2007

J Pharmacol Exp Ther

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Epoxyeicosatrienoic acids (EETs) have been reported to contract intralobar pulmonary arteries (PA) of the rabbit in a cyclooxygenase (COX)-dependent manner. In the present study, we observed that COX-1 and COX-2 isoforms were expressed in freshly isolated PA of healthy rabbits. We examined the hypothesis that both COX isoforms participate in 5,6-EET-induced contraction of rabbit intralobar PA. Selective inhibition of COX-1 with 300 nM 5-(4-chlorophenyl)-1-(4-methoxyphenyl)-3-(trifluoromethyl)-1H-pyrazole (SC-560) prevented 5,6-EET (1 ϫ 10 Ϫ8 -1 ϫ 10 Ϫ5 M)-induced contractions of isolated intralobar rabbit PA rings in a manner similar to that observed with the nonselective cyclooxygenase inhibitor indomethacin at 10 M. Selective inhibition of COX-2 with either 100 nM 5-bromo-2-(4-fluorophenyl)-3-(4-methylsulfonyl) thiophene (DUP-697) or 3 M N-(2-cyclohexyloxy-4-nitrophenyl) methanesulfonamide (NS-398) shifted the EC 50 value of 5,6-EET-induced PA contraction to the right but with considerably lower efficacy than SC-560. In rabbit PA, 5,6-EET-induced contraction was primarily dependent on COX-1 activity. Differential metabolism of 5,6-EET by COX-1 and COX-2 does not explain the primary dependence of PA contraction on COX-1 activity because 5,6-EET was metabolized similarly by both COX isoforms. COX-1 and -2 were expressed primarily in PA endothelium where COX-1 expression was dense and uniform, whereas COX-2 expression was sparse and nonuniform. 5,6-EET-induced PA contraction was endothelium-dependent. These results suggest that 5,6-EET-induced contraction is primarily dependent on COX-1 activity.

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Purification and Characterization of Prostaglandin H Synthase-2 from Sheep Placental Cotyledons

Cited by 110 publications

References 0 publications

Cox-2 inhibitors induce early c-Myc downregulation and lead to expression of differentiation markers in leukemia cells

Cox-2 inhibitors induce early c-Myc downregulation and lead to expression of differentiation markers in leukemia cells

Copper-Aspirin Complex Inhibits Cyclooxygenase-2 More Selectively than Aspirin

Cyclooxygenase (COX)-1 and COX-2 Participate in 5,6-Epoxyeicosatrienoic Acid-Induced Contraction of Rabbit Intralobar Pulmonary Arteries

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