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Johannes Berger - One of the best experts on this subject based on the ideXlab platform.
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homeostasis of phospholipids the level of phosphatidylEthanolamine tightly adapts to changes in Ethanolamine plasmalogens
Biochimica et Biophysica Acta, 2015Co-Authors: Fabian Dorninger, Alexander Brodde, Wilhelm W Just, Nancy Braverman, Britta Brügger, Ann B. Moser, Sonja Forsspetter, Johannes BergerAbstract:Ethanolamine plasmalogens constitute a group of ether glycerophospholipids that, due to their unique biophysical and biochemical properties, are essential components of mammalian cellular membranes. Their importance is emphasized by the consequences of defects in plasmalogen biosynthesis, which in humans cause the fatal disease rhizomelic chondrodysplasia punctata (RCDP). In the present lipidomic study, we used fibroblasts derived from RCDP patients, as well as brain tissue from plasmalogen-deficient mice, to examine the compensatory mechanisms of lipid homeostasis in response to plasmalogen deficiency. Our results show that phosphatidylEthanolamine (PE), a diacyl glycerophospholipid, which like Ethanolamine plasmalogens carries the head group Ethanolamine, is the main player in the adaptation to plasmalogen insufficiency. PE levels were tightly adjusted to the amount of Ethanolamine plasmalogens so that their combined levels were kept constant. Similarly, the total amount of polyunsaturated fatty acids (PUFAs) in Ethanolamine phospholipids was maintained upon plasmalogen deficiency. However, we found an increased incorporation of arachidonic acid at the expense of docosahexaenoic acid in the PE fraction of plasmalogen-deficient tissues. These data show that under conditions of reduced plasmalogen levels, the amount of total Ethanolamine phospholipids is precisely maintained by a rise in PE. At the same time, a shift in the ratio between ω-6 and ω-3 PUFAs occurs, which might have unfavorable, long-term biological consequences. Therefore, our findings are not only of interest for RCDP but may have more widespread implications also for other disease conditions, as for example Alzheimer's disease, that have been associated with a decline in plasmalogens.
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Homeostasis of phospholipids — The level of phosphatidylEthanolamine tightly adapts to changes in Ethanolamine plasmalogens
Biochimica et Biophysica Acta, 2014Co-Authors: Fabian Dorninger, Alexander Brodde, Sonja Forss-petter, Wilhelm W Just, Nancy Braverman, Britta Brügger, Ann B. Moser, Johannes BergerAbstract:Ethanolamine plasmalogens constitute a group of ether glycerophospholipids that, due to their unique biophysical and biochemical properties, are essential components of mammalian cellular membranes. Their importance is emphasized by the consequences of defects in plasmalogen biosynthesis, which in humans cause the fatal disease rhizomelic chondrodysplasia punctata (RCDP). In the present lipidomic study, we used fibroblasts derived from RCDP patients, as well as brain tissue from plasmalogen-deficient mice, to examine the compensatory mechanisms of lipid homeostasis in response to plasmalogen deficiency. Our results show that phosphatidylEthanolamine (PE), a diacyl glycerophospholipid, which like Ethanolamine plasmalogens carries the head group Ethanolamine, is the main player in the adaptation to plasmalogen insufficiency. PE levels were tightly adjusted to the amount of Ethanolamine plasmalogens so that their combined levels were kept constant. Similarly, the total amount of polyunsaturated fatty acids (PUFAs) in Ethanolamine phospholipids was maintained upon plasmalogen deficiency. However, we found an increased incorporation of arachidonic acid at the expense of docosahexaenoic acid in the PE fraction of plasmalogen-deficient tissues. These data show that under conditions of reduced plasmalogen levels, the amount of total Ethanolamine phospholipids is precisely maintained by a rise in PE. At the same time, a shift in the ratio between ω-6 and ω-3 PUFAs occurs, which might have unfavorable, long-term biological consequences. Therefore, our findings are not only of interest for RCDP but may have more widespread implications also for other disease conditions, as for example Alzheimer's disease, that have been associated with a decline in plasmalogens.
R F Witkamp - One of the best experts on this subject based on the ideXlab platform.
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docosahexaenoic acid and eicosapentaenoic acid are converted by 3t3 l1 adipocytes to n acyl Ethanolamines with anti inflammatory properties
Biochimica et Biophysica Acta, 2010Co-Authors: Michiel G J Balvers, Kitty C M Verhoeckx, Pierluigi Plastina, Heleen M Wortelboer, Jocelijn Meijerink, R F WitkampAbstract:n-3 PUFAs have beneficial health effects which are believed to be partly related to their anti-inflammatory properties, however the exact mechanisms behind this are unknown. One possible explanation could be via their conversion to N-acyl Ethanolamines (NAEs), which are known to possess anti-inflammatory properties. Using fatty acid precursors we showed that 3T3-L1 adipocytes are indeed able to convert docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) to their NAE derivatives docosahexaenoyl Ethanolamine (DHEA) and eicosapentaenoyl Ethanolamine (EPEA), respectively. This synthesis took place on top of an apparent background formation of these NAEs in standard culture medium. In addition we were able to demonstrate the presence of DHEA, but not of EPEA, in human plasma. DHEA and EPEA were found to decrease LPS induced adipocyte IL-6 and MCP-1 levels. Results of combined incubations with PPAR-γ and CB2 antagonists suggest a role of these receptors in mediating the reduction of IL-6 by DHEA. Our results are in line with the hypothesis that in addition to other pathways, formation of N-acyl Ethanolamines may contribute to the biological activity of n-3 PUFAs. Different targets, including the endocannabinoid system, may be involved in the immune-modulating activity of these "fish-oil-derived NAEs." © 2010 Elsevier B.V.
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development and validation of a quantitative method for the determination of 12 endocannabinoids and related compounds in human plasma using liquid chromatography tandem mass spectrometry
Journal of Chromatography B, 2009Co-Authors: Michiel G J Balvers, Kitty C M Verhoeckx, R F WitkampAbstract:A sensitive and specific LC-MS/MS method for the quantification of the endocannabinoids and related structures anandamide, 2-arachidonoyl glycerol, 2-arachidonyl glycerol ether, O-arachidonoyl ethanolamide, dihomo-γ-linolenoyl ethanolamide, docosatetraenoyl ethanolamide, N-arachidonoyl dopamine, N-arachidonyl glycine, N-oleoyl dopamine, oleoyl ethanolamide, palmitoyl ethanolamide, and stearoyl ethanolamide in human plasma was developed and validated. Compounds were extracted using acetonitrile followed by solid-phase extraction. Separation was performed on a Xterra C8 column using gradient elution coupled to a triple-quadrupole MS. LLOQ levels ranged from 0.02 to 1.75 μg/mL, LODs ranged from 0.0002 to 0.1266 ng/mL, and accuracies were >80% (except stearoyl ethanolamide at lowest spike level) at all spike levels. © 2009 Elsevier B.V. All rights reserved.
Fabian Dorninger - One of the best experts on this subject based on the ideXlab platform.
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homeostasis of phospholipids the level of phosphatidylEthanolamine tightly adapts to changes in Ethanolamine plasmalogens
Biochimica et Biophysica Acta, 2015Co-Authors: Fabian Dorninger, Alexander Brodde, Wilhelm W Just, Nancy Braverman, Britta Brügger, Ann B. Moser, Sonja Forsspetter, Johannes BergerAbstract:Ethanolamine plasmalogens constitute a group of ether glycerophospholipids that, due to their unique biophysical and biochemical properties, are essential components of mammalian cellular membranes. Their importance is emphasized by the consequences of defects in plasmalogen biosynthesis, which in humans cause the fatal disease rhizomelic chondrodysplasia punctata (RCDP). In the present lipidomic study, we used fibroblasts derived from RCDP patients, as well as brain tissue from plasmalogen-deficient mice, to examine the compensatory mechanisms of lipid homeostasis in response to plasmalogen deficiency. Our results show that phosphatidylEthanolamine (PE), a diacyl glycerophospholipid, which like Ethanolamine plasmalogens carries the head group Ethanolamine, is the main player in the adaptation to plasmalogen insufficiency. PE levels were tightly adjusted to the amount of Ethanolamine plasmalogens so that their combined levels were kept constant. Similarly, the total amount of polyunsaturated fatty acids (PUFAs) in Ethanolamine phospholipids was maintained upon plasmalogen deficiency. However, we found an increased incorporation of arachidonic acid at the expense of docosahexaenoic acid in the PE fraction of plasmalogen-deficient tissues. These data show that under conditions of reduced plasmalogen levels, the amount of total Ethanolamine phospholipids is precisely maintained by a rise in PE. At the same time, a shift in the ratio between ω-6 and ω-3 PUFAs occurs, which might have unfavorable, long-term biological consequences. Therefore, our findings are not only of interest for RCDP but may have more widespread implications also for other disease conditions, as for example Alzheimer's disease, that have been associated with a decline in plasmalogens.
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Homeostasis of phospholipids — The level of phosphatidylEthanolamine tightly adapts to changes in Ethanolamine plasmalogens
Biochimica et Biophysica Acta, 2014Co-Authors: Fabian Dorninger, Alexander Brodde, Sonja Forss-petter, Wilhelm W Just, Nancy Braverman, Britta Brügger, Ann B. Moser, Johannes BergerAbstract:Ethanolamine plasmalogens constitute a group of ether glycerophospholipids that, due to their unique biophysical and biochemical properties, are essential components of mammalian cellular membranes. Their importance is emphasized by the consequences of defects in plasmalogen biosynthesis, which in humans cause the fatal disease rhizomelic chondrodysplasia punctata (RCDP). In the present lipidomic study, we used fibroblasts derived from RCDP patients, as well as brain tissue from plasmalogen-deficient mice, to examine the compensatory mechanisms of lipid homeostasis in response to plasmalogen deficiency. Our results show that phosphatidylEthanolamine (PE), a diacyl glycerophospholipid, which like Ethanolamine plasmalogens carries the head group Ethanolamine, is the main player in the adaptation to plasmalogen insufficiency. PE levels were tightly adjusted to the amount of Ethanolamine plasmalogens so that their combined levels were kept constant. Similarly, the total amount of polyunsaturated fatty acids (PUFAs) in Ethanolamine phospholipids was maintained upon plasmalogen deficiency. However, we found an increased incorporation of arachidonic acid at the expense of docosahexaenoic acid in the PE fraction of plasmalogen-deficient tissues. These data show that under conditions of reduced plasmalogen levels, the amount of total Ethanolamine phospholipids is precisely maintained by a rise in PE. At the same time, a shift in the ratio between ω-6 and ω-3 PUFAs occurs, which might have unfavorable, long-term biological consequences. Therefore, our findings are not only of interest for RCDP but may have more widespread implications also for other disease conditions, as for example Alzheimer's disease, that have been associated with a decline in plasmalogens.
Zoltan Kiss - One of the best experts on this subject based on the ideXlab platform.
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phosphorylation of Ethanolamine methylEthanolamine and dimethylEthanolamine by overexpressed Ethanolamine kinase in nih 3t3 cells decreases the co mitogenic effects of Ethanolamines and promotes cell survival
FEBS Journal, 1998Co-Authors: Barbara Malewicz, Jagat J Mukherjee, Karan S Crilly, Wolfgang Baumann, Zoltan KissAbstract:: Ethanolamine (Etn), as well as its N-methyl (MeEtn) and N,N-dimethyl (Me2Etn) analogues, were recently shown to potentiate the stimulatory effect of insulin on DNA synthesis in serum-starved NIH 3T3 fibroblasts. In the present work we assessed the impact of the co-mitogenic effects of Etn and its methyl analogues on cell proliferation and cell survival, and examined whether the cell growth regulatory effects of these Ethanolamines involve an Etn-kinase-mediated phosphorylation step. For this purpose, NIH 3T3 sublines highly overexpressing Drosophila Etn kinase and an appropriate vector control line were utilized and the effects of Etn, MeEtn, Me2Etn, methylamine (MeNH2), and dimethylamine (Me2NH) were studied. 31P-NMR analysis of the water-soluble cell metabolites revealed that both MeEtn and Me2Etn, but not choline, are excellent substrates for the expressed Etn kinase. The methylated Ethanolamines (MeEtn and Me2Etn) and methylamines (MeNH2, Me2NH) were used as Etn models that can or cannot be phosphorylated, respectively. In serum-starved vector control cells, both MeNH2 (1 mM) and Me2NH (1 mM) were more effective than Etn in enhancing insulin-induced DNA synthesis, and both were almost as effective as MeEtn and Me2Etn. However, in the Etn kinase overexpressor cells the potentiating effects of Etn, MeEtn and Me2Etn, but not those of MeNH2 and Me2NH, were significantly reduced. Moreover, in the overexpressor cells, lower concentrations of Etn (50-200 microM) inhibited the combined mitogenic effects of Me2NH (1 mM) and insulin. These data are consistent with a mechanism in which the phosphorylated and non-phosphorylated Ethanolamines are negative and positive regulators of insulin-induced mitogenesis, respectively. After incubating the cells for 13 days in serum-free medium in 96-well microplates, there was a steady decrease in cell numbers in both cell lines. However, between 6-13 days, 0.1-1 mM MeEtn and, particularly, Me2Etn provided significant protection against cell death in the Etn kinase overexpressor cells. In vector control cells, only Me2Etn in combination with insulin had similar effects on cell survival. The data suggest that phosphorylated Ethanolamines may function as promoters of cell survival.
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protein kinase c inhibitors enhance the synergistic mitogenic effects of Ethanolamine analogues and insulin in nih 3t3 fibroblasts
Biochemical and Biophysical Research Communications, 1996Co-Authors: Zoltan Kiss, Karan S Crilly, Wayne B AndersonAbstract:Abstract MonomethylEthanolamine (1 mM) and dimethylEthanolamine (1 mM) stimulated DNA synthesis 10- and 15-fold, respectively, in NIH 3T3 fibroblasts. In addition, simultaneous treatments with insulin (500 nM) and methylated Ethanolamine analogues (1 mM or less) resulted in synergistic activation of DNA synthesis. The order of mitogenic potency of Ethanolamine analogues was dimethylEthanolamine > monomethylEthanolamine > Ethanolamine. Choline (1–5 mM) alone had no effect on DNA synthesis, but it increased the combined effects of lower concentrations of Ethanolamine analogues and insulin. The synergistic effects of Ethanolamine analogues, choline and insulin were considerably (1.7- to 1.9-fold) enhanced by GF 109203X (3 μM), a specific inhibitor of protein kinase C. The results suggest that Ethanolamine analogues enhance insulin-induced DNA synthesis by a mechanism which is inhibited by the protein kinase C system.
Alexander Brodde - One of the best experts on this subject based on the ideXlab platform.
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homeostasis of phospholipids the level of phosphatidylEthanolamine tightly adapts to changes in Ethanolamine plasmalogens
Biochimica et Biophysica Acta, 2015Co-Authors: Fabian Dorninger, Alexander Brodde, Wilhelm W Just, Nancy Braverman, Britta Brügger, Ann B. Moser, Sonja Forsspetter, Johannes BergerAbstract:Ethanolamine plasmalogens constitute a group of ether glycerophospholipids that, due to their unique biophysical and biochemical properties, are essential components of mammalian cellular membranes. Their importance is emphasized by the consequences of defects in plasmalogen biosynthesis, which in humans cause the fatal disease rhizomelic chondrodysplasia punctata (RCDP). In the present lipidomic study, we used fibroblasts derived from RCDP patients, as well as brain tissue from plasmalogen-deficient mice, to examine the compensatory mechanisms of lipid homeostasis in response to plasmalogen deficiency. Our results show that phosphatidylEthanolamine (PE), a diacyl glycerophospholipid, which like Ethanolamine plasmalogens carries the head group Ethanolamine, is the main player in the adaptation to plasmalogen insufficiency. PE levels were tightly adjusted to the amount of Ethanolamine plasmalogens so that their combined levels were kept constant. Similarly, the total amount of polyunsaturated fatty acids (PUFAs) in Ethanolamine phospholipids was maintained upon plasmalogen deficiency. However, we found an increased incorporation of arachidonic acid at the expense of docosahexaenoic acid in the PE fraction of plasmalogen-deficient tissues. These data show that under conditions of reduced plasmalogen levels, the amount of total Ethanolamine phospholipids is precisely maintained by a rise in PE. At the same time, a shift in the ratio between ω-6 and ω-3 PUFAs occurs, which might have unfavorable, long-term biological consequences. Therefore, our findings are not only of interest for RCDP but may have more widespread implications also for other disease conditions, as for example Alzheimer's disease, that have been associated with a decline in plasmalogens.
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Homeostasis of phospholipids — The level of phosphatidylEthanolamine tightly adapts to changes in Ethanolamine plasmalogens
Biochimica et Biophysica Acta, 2014Co-Authors: Fabian Dorninger, Alexander Brodde, Sonja Forss-petter, Wilhelm W Just, Nancy Braverman, Britta Brügger, Ann B. Moser, Johannes BergerAbstract:Ethanolamine plasmalogens constitute a group of ether glycerophospholipids that, due to their unique biophysical and biochemical properties, are essential components of mammalian cellular membranes. Their importance is emphasized by the consequences of defects in plasmalogen biosynthesis, which in humans cause the fatal disease rhizomelic chondrodysplasia punctata (RCDP). In the present lipidomic study, we used fibroblasts derived from RCDP patients, as well as brain tissue from plasmalogen-deficient mice, to examine the compensatory mechanisms of lipid homeostasis in response to plasmalogen deficiency. Our results show that phosphatidylEthanolamine (PE), a diacyl glycerophospholipid, which like Ethanolamine plasmalogens carries the head group Ethanolamine, is the main player in the adaptation to plasmalogen insufficiency. PE levels were tightly adjusted to the amount of Ethanolamine plasmalogens so that their combined levels were kept constant. Similarly, the total amount of polyunsaturated fatty acids (PUFAs) in Ethanolamine phospholipids was maintained upon plasmalogen deficiency. However, we found an increased incorporation of arachidonic acid at the expense of docosahexaenoic acid in the PE fraction of plasmalogen-deficient tissues. These data show that under conditions of reduced plasmalogen levels, the amount of total Ethanolamine phospholipids is precisely maintained by a rise in PE. At the same time, a shift in the ratio between ω-6 and ω-3 PUFAs occurs, which might have unfavorable, long-term biological consequences. Therefore, our findings are not only of interest for RCDP but may have more widespread implications also for other disease conditions, as for example Alzheimer's disease, that have been associated with a decline in plasmalogens.