Formation of antibodies to prostaglandins in the yolk of chicken eggs

Fertel, Richard H.; Yetiv, Jack Z.; Coleman, Marilyn A.; Schwarz, Roy D.; Greenwald, James E.; Bianchine, Joseph R.

doi:10.1016/0006-291x(81)91641-7

Cited by 57 publications

(9 citation statements)

References 8 publications

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“…Prostaglandin E 2 and 6-keto-PGF,, (the stable metabolite of prostacyclin) were not measured in the present study because the profiles of these prostaglandins have been previously reported to parallel that of PGF 2 ,, in IL-11p-stimulated luteal cells [16]. The crossreactivity of the antisera with other prostaglandins or steroids has been previously reported [21,22]. Intra-and interassay coefficients of variation for PGF 2 , were 11.5% and 16.3%, respectively; for P 4 , 16.9% and 23.0%, respectively.…”

Section: Methodsmentioning

confidence: 76%

Regulation of Prostaglandin Synthesis by Interleukin-1β in Cultured Bovine Luteal Cells1

Townson

Pate

1994

Biology of Reproduction

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Prostaglandins produced within the CL may serve as local modulators of CL function. The present study was designed to characterize the cellular mechanisms by which the cytokine interleukin-1 beta (IL-1 beta) stimulates prostaglandin production in cultured luteal cells. Cycloheximide (CHX) and actinomycin D (Act D) did not affect basal, but completely inhibited IL-1 beta-stimulated prostaglandin F2 alpha (PGF2 alpha) production (p < 0.05). The phospholipase A2 (PLA2) inhibitor, aristolochic acid (PLA2X), and the phospholipase C (PLC) inhibitor, compound 48/80 (PLCX), suppressed IL-1 beta-stimulated (p < 0.05), but not basal, PGF2 alpha production. The addition of exogenous arachidonic acid (AA) restored the stimulatory effect of IL-1 beta in PLCX-treated, but not in PLA2X-treated, cells, suggesting that PLA2 is a key regulatory point of IL-1 beta action. Chronic exposure of the luteal cells to IL-1 beta resulted in stimulatory effects beyond that of increasing AA availability, presumably by up-regulation of prostaglandin endoperoxide (PGH) synthase. Chronic exposure of luteal cells to IL-1 beta also inhibited progesterone production, but this effect appeared to be independent of endogenous PGF2 alpha production. The ability of IL-1 beta to comprehensively stimulate luteal PGF2 alpha production while inhibiting luteal progesterone production is suggestive that IL-1 beta may facilitate regression of the CL.

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Section: Methodsmentioning

confidence: 76%

Regulation of Prostaglandin Synthesis by Interleukin-1β in Cultured Bovine Luteal Cells1

Townson

Pate

1994

Biology of Reproduction

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“…Lipids were eluted with 100 ml each of the following solvents: chloroform (neutral lipids), methyl formate (prostaglandins and cerebrosides), acetone (remaining glycolipids), and methanol (phospholipids). Cholesterol was quantitated by the method of Bowman and Wolf (30) and prostaglandins were measured by radioimmunoassay (31). Phospholipids were separated by reactional twodimensional TLC (32), visualized by iodine vapors, the spots were scraped, and phosphorus was quantitated by the method of Rouser et al (26).…”

Section: Methodsmentioning

confidence: 99%

Membrane lipid changes in laminectomized and traumatized cat spinal cord.

Demediuk¹,

Saunders²,

Anderson³

et al. 1985

Proc. Natl. Acad. Sci. U.S.A.

157

105

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Free fatty acid (FFA), diacyiglycerol (acyl2-Gro), icosanoid, phospholipid, and cholesterol levels were measured in samples of cat spinal cord (L2) that were frozen in situ (i) with vertebrae intact, (ii) at various times after laminectomy, and (iu) at various times after laminectomy with compression trauma to the spinal cord. Tissue samples either were grossly dissected into gray and white portions prior to FFA and acyl2Gro analysis or were used whole for the other lipid types. Gray matter total FFA and acyl2Gro values were abnormally high in samples frozen with vertebrae intact and in those frozen 10 min after laminectomy. This indicates that the surgical procedures resulted in some perturbation of spinal cord lipid metabolism. If the experimental animals were allowed to recover for 90 min after laminectomy, the gray matter FFA and acyl2Gro levels were greatly reduced. Compression of the spinal cord with a 170-g weight for 1, 3, or 5mm (following 90 min of recovery after laminectomy) caused significant elevations of total FFA, acyl2Gro, icosanoids, and phosphatidic acid and significant decreases in ethalamine plasmalogens and cholesterol. Among the total FFA, arachidonic acid was found to have the largest relative increase. Comparisons of gray and white matter demonstrate that, in general, changes in white matter FFA and acyl2Gro were similar to those seen in gray matter. However, the increases in white matter levels of FFA and acyl2Gro were delayed, occurring after the elevations in gray matter. For some FFA (e.g., arachidonate), the rise in white matter occurred as gray matter levels were decreasing. This suggests that the initial alteration in spinal cord lipid metabolism after trauma was in gray matter but, with time, spread radially into white matter.

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“…Radioimmunoassay (RIA) PGE 2 was determined by collecting culture media from cells seeded in 24-well plates at 5 ϫ 10 5 cells/well in 0.5 mL of DMEM followed by RIA analysis according to the method of Fertel et al [30]. Antibodies used in this procedure do not cross-react with arachidonic acid or any of the other cyclooxygenase products (unpublished results).…”

Section: Sodium Dodecyl Sulfate-polyacrylamide Gel Electrophoresis (Smentioning

confidence: 99%

Blockade of nitric oxide formation down-regulates cyclooxygenase-2 and decreases PGE2 biosynthesis in macrophages

Perkins

Kniss

1999

Journal of Leukocyte Biology

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Elevated levels of nitric oxide (NO*) produced by expression of inducible nitric oxide synthase (iNOS/NOS type 2) and high levels of prostaglandins (PGs) generated by expression of inducible cyclooxygenase (COX-2/PGH2 synthase-2) are important mediators of immune and inflammatory responses. Previous studies have shown that endogenous levels of NO* can influence the formation of PGs. We examined the mechanism by which NO* regulates PG biosynthesis in macrophages. Treatment of a murine macrophage cell line (ANA-1) with lipopolysaccharide (LPS, 10 ng/mL) and interferon-gamma (IFN-gamma, 10 U/mL) for 20 h elicited high levels of nitrite (NO2-) and prostaglandin E2 (PGE2) that were inhibited in a dose-dependent fashion by the NOS inhibitor, aminoguanidine (AG), with IC50 values of 15.06 and 0.38 microM for NO2- and PGE2, respectively. Stimulation of cultures with LPS and IFN-gamma for 20 h induced de novo iNOS protein expression that was not altered by the addition of AG (0.1, 10, or 1000 microM). In contrast, treatment of cultures with LPS and IFN-gamma for 20 h promoted COX-2 mRNA and protein expression that were decreased in a dose-dependent fashion by AG (P < 0.05 with 10 and 1000 microM). LPS and IFN-gamma-induced COX-2 protein expression was not decreased in cultures treated with AG for 2 h, illustrating that AG does not inhibit the formation of COX-2 protein. Analysis of partially purified enzyme extracts demonstrated that AG did not directly inhibit the enzymatic activity of COX. Additional experiments revealed that NO* donors (S-nitroso-N-aceytl-D-L-pencillamine, SNAP, at 0.1, 10, and 1000 microM) did not induce de novo COX-2 protein expression or potentiate COX-2 expression in cells treated with LPS and/or IFN-gamma. Our results suggest that, while endogenous NO* is not required for de novo COX-2 mRNA and protein expression, NO* is necessary for maintaining prolonged COX-2 gene expression.

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Formation of antibodies to prostaglandins in the yolk of chicken eggs

Cited by 57 publications

References 8 publications

Regulation of Prostaglandin Synthesis by Interleukin-1β in Cultured Bovine Luteal Cells1

Regulation of Prostaglandin Synthesis by Interleukin-1β in Cultured Bovine Luteal Cells1

Membrane lipid changes in laminectomized and traumatized cat spinal cord.

Blockade of nitric oxide formation down-regulates cyclooxygenase-2 and decreases PGE2 biosynthesis in macrophages

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