Lipidomics reveals membrane lipid remodelling and release of potential lipid mediators during early stress responses in a murine melanoma cell line |
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Authors: | Gá bor Balogh,Má ria Pé ter,Gerhard Liebisch,Ibolya Horvá th,Zsolt Tö rö k,Enikő Nagy,Andriy Maslyanko,Sá ndor Benkő,Gerd Schmitz,John L. Harwood,Lá szló Ví gh |
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Affiliation: | 1. Institute of Biochemistry, Biological Research Centre, Hungarian Academy of Sciences, Szeged, Hungary;2. University of Regensburg, Regensburg, Germany;3. University of Szeged, Faculty of Medicine, 1st Department of Medicine, Szeged, Hungary;4. School of Biosciences, Cardiff University, Cardiff CF10 3AX, Wales, UK |
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Abstract: | Membranes are known to respond rapidly to various environmental perturbations by changing their composition and microdomain organization. In previous work we showed that a membrane fluidizer benzyl alcohol (BA) could mimic the effects of heat stress and enhance heat shock protein synthesis in different mammalian cells. Here we explore heat- and BA-induced stress further by characterizing stress-induced membrane lipid changes in mouse melanoma B16 cells. Lipidomic fingerprints revealed that membrane stress achieved either by heat or BA resulted in pronounced and highly specific alterations in lipid metabolism. The loss in polyenes with the concomitant increase in saturated lipid species was shown to be a consequence of the activation of phopholipases (mainly phopholipase A2 and C). A phospholipase C–diacylglycerol lipase–monoacylglycerol lipase pathway was identified in B16 cells and contributed significantly to the production of several lipid mediators upon stress including the potent heat shock modulator, arachidonic acid. The accumulation of cholesterol, ceramide and saturated phosphoglyceride species with raft-forming properties observed upon both heat and BA treatments of B16 cells may explain the condensation of ordered plasma membrane domains previously detected by fluorescence microscopy and may serve as a signalling platform in stress responses or as a primary defence mechanism against the noxious effects of stresses. |
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Keywords: | AA, arachidonic acid BA, benzyl alcohol CE, cholesteryl ester Cer, ceramide Chol, cholesterol DAG, diacylglycerol ESI-MS/MS, electrospray ionization tandem mass spectrometry FA, fatty acid FAAH, fatty acid amide hydrolase FAME, fatty acid methyl ester FFA, free (non-esterified) fatty acid GC-MS, gas chromatography-mass spectrometry HSF1, heat shock factor1 Hsp, heat shock protein IP3, inositol-1,4,5-trisphosphate LPC, lysophosphatidylcholine MAFP, methyl arachidonyl fluorophosphonate MAG, monoacylglycerol MDR, multidrug resistant PCA, principal component analysis PC and PC-O, diacyl and 1-alkyl-2-acyl species of phosphatidylcholine, respectively PC1, PC2 and PC3, first, second and third principal components, respectively PE, diacyl phosphatidylethanolamine PE-P, 1-(1Z-alkenyl)-2-acyl species of PE PG, phosphatidylglycerol PI, phosphatidylinositol PKC, protein kinase C PLA2, phospholipase A2 PLC, phospholipase C PS, phosphatidylserine SFA, MUFA and PUFA, saturated, monounsaturated and polyunsaturated FAs, respectively SM, sphingomyelin THL, tetrahydrolipstatin TPL, total polar lipid fraction |
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