The stability of dilute solutions of prostaglandins E1, E2, F1aand F2a

Karim, S. M. M.; Devlin, Jean; Hillier, Keith

doi:10.1016/0014-2999(68)90028-9

Cited by 42 publications

(5 citation statements)

References 7 publications

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“…PGE 2 levels continued to accumulate up to 24 h after stimulation. Owing to the remarkable chemical stability of PGE 2 (50), levels accumulate in culture media over the time course of production ( Fig. 1A).…”

Section: Tnf Induces Pge 2 Production In L929 Cells Via Induction Of mentioning

confidence: 99%

The sphingosine kinase 1/sphingosine‐1‐phosphate pathway mediates COX‐2 induction and PGE₂production in response to TNF‐α

et al. 2003

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In this study we addressed the role of sphingolipid metabolism in the inflammatory response. In a L929 fibroblast model, tumor necrosis factor-alpha (TNF) induced prostaglandin E2 (PGE2) production by 4 h and cyclooxygenase-2 (COX-2) induction as early as 2 h. This TNF-induced PGE2 production was inhibited by NS398, a COX-2 selective inhibitor. GC-MS analysis revealed that only COX-2-generated prostanoids were produced in response to TNF, thus providing further evidence of COX-2 selectivity. As sphingolipids have been implicated in mediating several actions of TNF, their role in COX-2 induction and PGE2 production was evaluated. Sphingosine-1-phosphate (S1P) induced both COX-2 and PGE2 in a dose-responsive manner with an apparent ED50 of 100-300 nM. The related sphingolipid sphingosine also induced PGE2, though with much less efficacy. TNF induced a 3.5-fold increase in sphingosine-1-phosphate levels at 10 min that rapidly returned to baseline by 40 min. Small interfering RNAs (siRNAs) directed against mouse SK1 decreased (typically by 80%) SK1 protein and inhibited TNF-induced SK activity. Treatment of cells with RNAi to SK1 but not SK2 almost completely abolished the ability of TNF to induce COX-2 or generate PGE2. By contrast, cells treated with RNAi to S1P lyase or S1P phosphatase enhanced COX-2 induction leading to enhanced generation of PGE2. Treatment with SK1 RNAi also abolished the effects of exogenous sphingosine and ceramide on PGE2, revealing that the action of sphingosine and ceramide are due to intracellular metabolism into S1P. Collectively, these results provide novel evidence that SK1 and S1P are necessary for TNF to induce COX-2 and PGE2 production. Based on these findings, this study indicates that SK1 and S1P could be implicated in pathological inflammatory disorders and cancer.

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Section: Tnf Induces Pge 2 Production In L929 Cells Via Induction Of mentioning

confidence: 99%

The sphingosine kinase 1/sphingosine‐1‐phosphate pathway mediates COX‐2 induction and PGE₂production in response to TNF‐α

et al. 2003

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“…Prostaglandins were determined without using any extraction or separation procedures. Therefore it must be concluded that these prostaglandins contained prostaglandins of the A, B, and E series but not the F series with alkaline stability (14). Thus, prostaglandin determined by the present radioimmunoassay is represented as "prostaglandins.…”

Section: Methodsmentioning

confidence: 72%

Changes in Prostaglandin Levels in Cultures of SV40‐Transformed Macrophage Cell Lines in Relation to Their Phenotypic Expression

Tanigawa

Suzuki

Takayama

et al. 1982

Microbiology and Immunology

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A radioimmunoassay was performed to determine the total amounts of the A, B, and E series prostaglandins (prostaglandins) in culture fluids of simian virus 40 (SV40)-transformed mouse clonal macrophages, line 28-12, and its subline, 28-12(Ara). When the proportion of phagocytic cells in confluent 28-12 cell cultures increased, the prostaglandin levels in the culture fluids decreased. On the other hand, stably phagocytic 28-12(Ara) cells, which were derived from 28-12 cells and which had a reduced growth rate, did not release prostaglandins under the usual culture conditions; however, when they were treated with lipopolysaccharide or streptococcal preparation OK-432, large amounts of prostaglandins were released. In contrast, nonphagocytic cell populations in the cultures of 28-12 cells were not responsive to the drug treatment. These results suggest that there is a correlation between the phenotypic change from the nonphagocytic to the phagocytic state and a decrease in prostaglandin levels in culture fluids, and indicate that phagocytic cells are responsive to prostaglandin inducers, whereas nonphagocytic cells are not.

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“…has shown that the coral active fraction co-runs with PGF2a. A comparison of the stability of hatching substance (Crisp & Spencer 1958) and prostaglandins of the F-series (Karim et al 1968) in solutions of various pH is also illuminati substance, PGFlot and PGF2a all exhibit a loss in smooth muscle stimulating activity if held in solution below pH 3. Furthermore, solutions of these compounds are all stable between pH 5 and 11.…”

Section: Identity Of the Hatching Substancementioning

confidence: 99%

“…light, whereas hatching substance in the purest form we achieved does. Further, there is little loss in smooth muscle-stimulating activity of PGFla and no loss in activity of PGF2(X when heated at 110 °C and 68950 Pa for 1 h (Karim al. 1968); the activity of hatching substance is destroyed by prolonged heating at 100 °C and so presumably would also be destroyed by autoclaving.…”

Section: Identity Of the Hatching Substancementioning

confidence: 99%

The hatching substance of the barnacle, balanus balanoides (L.)

1985

Proc. R. Soc. Lond. B.

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Hatching substance has been extracted from the barnacle, Balanus balanoides, and partly purified by thin layer chromatography. Several lines of evidence indicate that hatching substance is a prosta-glandin. First, the compound is extracted by a prostaglandin extraction procedure. Secondly, a fraction isolated from the dried cortex of the gorgonian coral, Plexaura homomalla , which stimulates barnacle eggs to hatch, co-migrates with hatching substance on thin layer chromatography plates. Acetylsalicylic acid (aspirin), which blocks the enzymic production of prostaglandins, prevents the formation of hatching substance. In contrast, indomethacin, which is a potent inhibitor of the mammalian cyclo-oxygenase, is without effect on the biosynthesis of hatching substance. Dopamine mimics the effect of hatching substance between the concentrations of 2.5 x 10 -3 M and 8.4 x 10 -5 M. Although dopamine is not the hatching substance per se , it is possible that this compound is implicated in the hatching process.

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The stability of dilute solutions of prostaglandins E1, E2, F1aand F2a

Cited by 42 publications

References 7 publications

The sphingosine kinase 1/sphingosine‐1‐phosphate pathway mediates COX‐2 induction and PGE₂production in response to TNF‐α

The sphingosine kinase 1/sphingosine‐1‐phosphate pathway mediates COX‐2 induction and PGE₂production in response to TNF‐α

Changes in Prostaglandin Levels in Cultures of SV40‐Transformed Macrophage Cell Lines in Relation to Their Phenotypic Expression

The hatching substance of the barnacle, balanus balanoides (L.)

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The stability of dilute solutions of prostaglandins E1, E2, F1aand F2a

Cited by 42 publications

References 7 publications

The sphingosine kinase 1/sphingosine‐1‐phosphate pathway mediates COX‐2 induction and PGE2production in response to TNF‐α

The sphingosine kinase 1/sphingosine‐1‐phosphate pathway mediates COX‐2 induction and PGE2production in response to TNF‐α

Changes in Prostaglandin Levels in Cultures of SV40‐Transformed Macrophage Cell Lines in Relation to Their Phenotypic Expression

The hatching substance of the barnacle, balanus balanoides (L.)

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The sphingosine kinase 1/sphingosine‐1‐phosphate pathway mediates COX‐2 induction and PGE₂production in response to TNF‐α

The sphingosine kinase 1/sphingosine‐1‐phosphate pathway mediates COX‐2 induction and PGE₂production in response to TNF‐α