Receptor-Mediated Degradation of Choline Plasmalogens and Glycerophospholipid Methylation: A New Hypothesis

Horrocks, Lloyd A.; Harder, Hubert W.; Mozzi, Rita; Goracci, G; Francescangeli, Ermelinda; Porcellati, Serena; Nenci, Giuseppe G.

doi:10.1007/978-1-4684-5212-9_85

Cited by 16 publications

(12 citation statements)

References 14 publications

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“…It has been reported that platelet PlasCho can be synthesized from the corresponding ethanolamine derivatives by methylation [34] but we have no direct evidence for correlating plasmalogen methylation with the release of arachidonic acid after the stimulation of platelets with thrombin. However, our data are consistent with the hypothesis that PlasCho participate somehow to the changes which take place at membrane level immediately after platelets are stimulated with thrombin [35]. In fact, there is a significant increase of the labeling of PlasCho up to about 20 sec after the addition of the agonist and it is interesting that AD 6 exert a certain influence on PlasCho metabolism expecially during the first period after the stimulation with thrombin.…”

Section: Discussionsupporting

confidence: 92%

The coumarin derivative AD6 inhibits the release of arachidonic acid by interfering with phospholipase A2 activity in human platelets stimulated with thrombin

et al. 1990

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AD6 is a coumarin derivative which is able to inhibit platelet aggregation and release due to various agonists as adrenaline, PAF, Ca++ ionophore and others. It has been demonstrated that this compound reduces the production of free arachidonate and diglyceride from human platelets pulse-labeled with radioactive arachidonic acid thus suggesting a possible interference with the activity of phospholipase A2 and/or phospholipase C. The present report indicates that the drug has no effect on the increase of the labeling of phosphatidic acid which takes place when platelets pulse-labeled with arachidonic acid are stimulated with thrombin. Furthermore, AD6 is not able to cause changes on the metabolism of phosphoinositides monitored using platelets pre-labeled with [3H] inositol. These observations exclude the possibility that AD6 interferes with phospholipase C activity. Experiments with platelets pulse-labeled with arachidonate suggest that AD6 inhibits phospholipase(s) A2 activity or modulate negatively one or more processes involved in its activation.

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Section: Discussionsupporting

confidence: 92%

The coumarin derivative AD6 inhibits the release of arachidonic acid by interfering with phospholipase A2 activity in human platelets stimulated with thrombin

et al. 1990

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“…The effects of L-and I-FABP expression on plasmalogen levels were determined. [Plasmalogens are phospholipids containing a vinyl ether linkage in the sn-1 position that are synthesized by steps involving both peroxisomes and ER; they have a role in lipid-mediated signal transduction (42)(43)(44)(45)]. In I-FABP-expressing cells, ethanolamine plasmalogen (PlsEtn) mass was increased 1.1-fold in these cells (Table 2).…”

Section: Resultsmentioning

confidence: 95%

“…Clearly, there was a profound effect on plasmalogen biosynthesis, with the increase in PlsCho proportions suggesting an increase in the utilization of PlsEtn to form the PlsCho (49,50). This increase in PlsCho proportions is important as PlsCho is the active plasmalogen pool involved in signal transduction (42)(43)(44)50,51).…”

Section: Discussionmentioning

confidence: 94%

“…Thus, by analyzing the ChoGpl and EtnGpl subclasses, it became evident that these proteins elevated both the acid-stable and acid-labile fractions relative to the control, indicating I-and L-FABP facilitated not only plasmalogen biosynthesis but also PtdEtn and PtdCho synthesis. Because plasmalogens have a role in lipid-mediated signal transduction (42)(43)(44), FABP may support not only the synthesis of PtdIns but also of other phospholipids involved in cell signaling.…”

Section: Discussionmentioning

confidence: 99%

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Liver and intestinal fatty acid‐binding protein expression increases phospholipid content and alters phospholipid fatty acid composition in L‐cell fibroblasts

Murphy

Prows

Stiles

et al. 2000

Lipids

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Although fatty acid-binding proteins (FABP) differentially affect fatty acid uptake, nothing is known regarding their role(s) in determining cellular phospholipid levels and phospholipid fatty acid composition. The effects of liver (L)- and intestinal (I)-FABP expression on these parameters were determined using stably transfected L-cells. Expression of L- and I-FABP increased cellular total phospholipid mass (nmol/mg protein) 1.7- and 1.3-fold relative to controls, respectively. L-FABP expression increased the masses of choline glycerophospholipids (ChoGpl) 1.5-fold, phosphatidylserine (PtdSer) 5.6-fold, ethanolamine glycerophospholipids 1.4-fold, sphingomyelin 1.7-fold, and phosphatidylinositol 2.6-fold. In contrast, I-FABP expression only increased the masses of ChoGpl and PtdSer, 1.2- and 3.1-fold, respectively. Surprisingly, both L- and I-FABP expression increased ethanolamine plasmalogen mass 1.6- and 1.1-fold, respectively, while choline plasmalogen mass was increased 2.3- and 1.7-fold, respectively. The increase in phospholipid levels resulted in dramatic 48 and 33% decreases in the cholesterol-to-phospholipid ratio in L- and I-FABP expressing cells, respectively. L-FABP expression generally increased polyunsaturated fatty acids, primarily by increasing 20:4n-6 and 22:6n-3, while decreasing 18:1n-9 and 16:1n-7. I-FABP expression generally increased only 20:4n-6 proportions. Hence, expression of both I- and L-FABP differentially affected phospholipid mass, class composition, and acyl chain composition. Although both proteins enhanced phospholipid synthesis, the effect of L-FABP was much greater, consistent with previous work suggesting that these two FABP differentially affect lipid metabolism.

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“…An important and distinctive component in brain membranes are the plasmalogens [47], which are putative signaling molecules [58-60]. Plasmalogens are especially enriched in myelin were ethanolamine plasmalogen account for 70-80% of total EtnGpl and for 12% of the total myelin phospholipid [61].…”

Section: Discussionmentioning

confidence: 99%

Prenatal Ethanol Exposure Increases Brain Cholesterol Content in Adult Rats

Barceló‐Coblijn

Wold

Ren

et al. 2013

Lipids

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Fetal alcohol syndrome is the most severe expression of the fetal alcohol spectrum disorders (FASD). Although alterations in fetal and neonate brain fatty acid composition and cholesterol content is known to change in animal models of FASD, the persistence of these alterations into adulthood is unknown. To address this question, we determined the effect of prenatal ethanol exposure on individual phospholipid class fatty acid composition, individual phospholipid class mass, and cholesterol mass in brains from 25-week-old rats that were exposed to ethanol during gestation beginning at gestational day 2. While total phospholipid mass was unaffected, phosphatidylinositol and cardiolipin mass was decreased 14 and 43%, respectively. Exposure to prenatal ethanol modestly altered brain phospholipid fatty acid composition, and the most consistent change was a significant 1.1-fold increase in total PUFA, in the n-3/n-6 ratio, and in the 22:6 n-3 content in ethanolamine glycerophospholipids and in phosphatidylserine. In contrast, prenatal ethanol consumption significantly increased brain cholesterol mass 1.4-fold and the phospholipid to cholesterol ratio was significantly increased 1.3-fold. These results indicate that brain cholesterol mass was significantly increased in adult rats exposed prenatally to ethanol, but changes in phospholipid mass and phospholipid fatty acid composition were extremely limited. Importantly, suppression of post-natal ethanol consumption was not sufficient to reverse the large increase in cholesterol observed in the adult rats.

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Receptor-Mediated Degradation of Choline Plasmalogens and Glycerophospholipid Methylation: A New Hypothesis

Cited by 16 publications

References 14 publications

The coumarin derivative AD6 inhibits the release of arachidonic acid by interfering with phospholipase A2 activity in human platelets stimulated with thrombin

The coumarin derivative AD6 inhibits the release of arachidonic acid by interfering with phospholipase A2 activity in human platelets stimulated with thrombin

Liver and intestinal fatty acid‐binding protein expression increases phospholipid content and alters phospholipid fatty acid composition in L‐cell fibroblasts

Prenatal Ethanol Exposure Increases Brain Cholesterol Content in Adult Rats

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