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Your search keyword '"prostaglandin e-2"' showing total 2 results
Start Over Descriptor "prostaglandin e-2" Journal journal of lipid research
2 results on '"prostaglandin e-2"'

1. PGE2 release is independent of upregulation of Group V phospholipase A2 during long-term stimulation of P388D1 cells with LPS 1

Author

Kessen, Ursula A, Schaloske, Ralph H, Stephens, Daren L, Lucas, Karin Killermann, and Dennis, Edward A

Subjects
Medical Physiology, Biomedical and Clinical Sciences, Animals, Arachidonic Acid, Cell Line, Culture Media, Cyclooxygenase 2, DNA, Complementary, Dinoprostone, Eicosanoids, Enzyme Inhibitors, Group V Phospholipases A2, Immunoblotting, Indoles, Lipids, Lipopolysaccharides, Macrophages, Mice, Oligonucleotides, Antisense, Phospholipases A, Phospholipases A2, Pyrrolidines, RNA, RNA, Messenger, Reverse Transcriptase Polymerase Chain Reaction, Time Factors, Transfection, Up-Regulation, antisense inhibitor, macrophage, lipopolysaccharide, prostaglandin E-2, arachidonic acid, eicosanoid, Biochemistry and Cell Biology, Medical Biochemistry and Metabolomics, Biochemistry & Molecular Biology, Biochemistry and cell biology, Medical biochemistry and metabolomics
Abstract

P388D1 cells release arachidonic acid (AA) and produce prostaglandin E2 (PGE2) upon long-term stimulation with lipopolysaccharide (LPS). The cytosolic Group IVA (GIVA) phospholipase A2 (PLA2) has been implicated in this pathway. LPS stimulation also results in increased expression and secretion of a secretory PLA2, specifically GV PLA2. To test whether GV PLA2 contributes to PGE2 production and whether GIVA PLA2 activation increases the expression of GV PLA2, we utilized the specific GIVA PLA2 inhibitor pyrrophenone and second generation antisense oligonucleotides (AS-ONs) designed to specifically inhibit expression and activity of GV PLA2. Treatment of P388D1 cells with antisense caused a marked decrease in basal GV PLA2 mRNA and prevented the LPS-induced increase in GV PLA2 mRNA. LPS-stimulated cells release active GV PLA2 into the medium, which is inhibited to background levels by antisense treatment. However, LPS-induced PGE2 release by antisense-treated cells and by control cells are not significantly different. Collectively, the results suggest that the upregulation of GV PLA2 during long-term LPS stimulation is not required for PGE2 production by P388D1 cells. Experiments employing pyrrophenone suggested that GIVA PLA2 is the dominant player involved in AA release, but it appears not to be involved in the regulation of LPS-induced expression of GV PLA2 or cyclooxygenase-2.

Published
2005

2. Aging bone marrow mesenchymal stromal cells have altered membrane glycerophospholipid composition and functionality[S]

Author

Dario Greco, Reijo Käkelä, Sofia Oja, Saara Laitinen, Matti Korhonen, Päivi Saavalainen, Amarjit Parmar, Lotta Kilpinen, Janne Nikkilä, Feven Tigistu-Sahle, Petri Lehenkari, Biosciences, Physiology and Neuroscience (-2020), Research Programs Unit, Research Programme of Molecular Medicine, Haartman Institute (-2014), Department of Medical and Clinical Genetics, Department of Anatomy, Medicum, Immunobiology Research Program, Functional Lipidomics Group, and Immunomics

Subjects
Aging, PROSTAGLANDIN E-2, Biochemistry, chemistry.chemical_compound, 0302 clinical medicine, Endocrinology, Cells, Cultured, Research Articles, mesenchymal stem cell, mass spectrometry, 0303 health sciences, glycerophospholipid profile, Phosphatidylserine, Telomere, docosahexaenoic acid, QUANTITATIVE-ANALYSIS, Cell biology, 030220 oncology & carcinogenesis, SIGNALING PATHWAY, Stem cell, STEM-CELLS, Stromal cell, Chromatography, Gas, Docosahexaenoic Acids, education, Blotting, Western, Glycerophospholipids, QD415-436, Biology, 03 medical and health sciences, arachidonic acid, Humans, Phosphatidylinositol, PROTEIN-KINASE-C, TANDEM MASS-SPECTROMETRY, 030304 developmental biology, Phosphatidylethanolamine, FATTY-ACID, INFLAMMATORY RESPONSE, Mesenchymal stem cell, Lipid metabolism, Mesenchymal Stem Cells, Cell Biology, Lipid signaling, Lipid Metabolism, PHOSPHOLIPASE A(2), chemistry, PLASMA-MEMBRANE, 1182 Biochemistry, cell and molecular biology, lipid signaling, 3111 Biomedicine
Abstract

Human mesenchymal stem/stromal cells (hMSC) are increasingly used in advanced cellular therapies. The clinical use of hMSCs demands sequential cell expansions. As it is well established that membrane glycerophospholipids (GPL) provide precursors for signaling lipids that modulate cellular functions, we studied the effect of the donor's age and cell doublings on the GPL profile of human bone marrow MSC (hBMSC). The hBMSCs, which were harvested from five young and five old adults, showed clear compositional changes during expansion seen at the level of lipid classes, lipid species, and acyl chains. The ratio of phosphatidylinositol to phosphatidylserine increased toward the late-passage samples. Furthermore, 20:4n-6-containing species of phosphatidylcholine and phosphatidylethanolamine accumulated while the species containing monounsaturated fatty acids (FA) decreased during passaging. Additionally, in the total FA pool of the cells, 20:4n-6 increased, which happened at the expense of n-3 polyunsaturated FAs, especially 22:6n-3. The GPL and FA correlated with the decreased immunosuppressive capacity of hBMSCs during expansion. Our observations were further supported by alterations in the gene expression levels of several enzymes involved in lipid metabolism and immunomodulation. The results show that extensive expansion of hBMSCs harmfully modulates membrane GPLs, affecting lipid signaling and eventually impairing functionality.

Published
2013

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