2n-fatty acids from phosphatidylcholine label sphingolipids—A novel role of phospholipase A2?

Meyer, Sybille G.E.; Karow, Werner; Groot, Herbert de

doi:10.1016/j.bbalip.2005.04.008

Cited by 6 publications

(4 citation statements)

References 44 publications

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“…Stimulators of ceramide formation in erythrocytes include platelet activating factor (PAF), which is generated by a pohospholipase A2 [38]. In other cell types Aristolochic Acid has been shown to inhibit phospholipase A2 [39,40]. It remains to be shown whether Aristolochic Acid stimulates ceramide formation in other cell types.…”

Section: Discussionmentioning

confidence: 99%

Aristolochic Acid Induced Suicidal Erythrocyte Death

Malik

Bissinger²,

Calabrò³

et al. 2014

Kidney Blood Press Res

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Section: Discussionmentioning

confidence: 99%

Aristolochic Acid Induced Suicidal Erythrocyte Death

Malik

Bissinger²,

Calabrò³

et al. 2014

Kidney Blood Press Res

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“…Aristolochic acid has a long track record as broad spectrum PLA 2 inhibitor [54-56]. Other than an extensive literature on the compound’s genotoxic effects that are associated with its ability to form aristolactam-DNA adducts [57,58], we are not aware of reports of non-specific activities.…”

Section: Discussionmentioning

confidence: 99%

Evidence for inflammation-mediated memory dysfunction in gastropods: putative PLA2and COX inhibitors abolish long-term memory failure induced by systemic immune challenges

et al. 2013

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BackgroundPrevious studies associate lipid peroxidation with long-term memory (LTM) failure in a gastropod model (Lymnaea stagnalis) of associative learning and memory. This process involves activation of Phospholipase A2 (PLA2), an enzyme mediating the release of fatty acids such as arachidonic acid that form the precursor for a variety of pro-inflammatory lipid metabolites. This study investigated the effect of biologically realistic challenges of L. stagnalis host defense response system on LTM function and potential involvement of PLA2, COX and LOX therein.ResultsSystemic immune challenges by means of β-glucan laminarin injections induced elevated H2O2 release from L. stagnalis circulatory immune cells within 3 hrs of treatment. This effect dissipated within 24 hrs after treatment. Laminarin exposure has no direct effect on neuronal activity. Laminarin injections disrupted LTM formation if training followed within 1 hr after injection but had no behavioural impact if training started 24 hrs after treatment. Intermediate term memory was not affected by laminarin injection. Chemosensory and motor functions underpinning the feeding response involved in this learning model were not affected by laminarin injection. Laminarin’s suppression of LTM induction was reversed by treatment with aristolochic acid, a PLA2 inhibitor, or indomethacin, a putative COX inhibitor, but not by treatment with nordihydro-guaiaretic acid, a putative LOX inhibitor.ConclusionsA systemic immune challenge administered shortly before behavioural training impairs associative LTM function in our model that can be countered with putative inhibitors of PLA2 and COX, but not LOX. As such, this study establishes a mechanistic link between the state of activity of this gastropod’s innate immune system and higher order nervous system function. Our findings underwrite the rapidly expanding view of neuroinflammatory processes as a fundamental, evolutionary conserved cause of cognitive and other nervous system disorders.

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“…PtdCho supplies the phosphocholine moiety for sphingomyelin synthesis (Hannun and Obeid, 2002) and PtdEtn can be synthesized from the degradation product of sphingosine, phosphoethanolamine (Smith and Merrill, 1995). Moreover, sn ‐2 fatty acids from PtdCho can be used for the synthesis of sphingoid base and ceramide (Meyer et al, 2005). Collective evidence suggests that metabolites of glycerophospholipid metabolism modulate sphingolipid degradation and lipid mediators of sphingolipid metabolism regulate activities of PLA 2 and cyclooxygenases (Farooqui et al, 2000b, 2006a).…”

Section: Physiologic and Pathophysiologic Effects Of Ceramide And Itsmentioning

confidence: 99%

Interactions between neural membrane glycerophospholipid and sphingolipid mediators: A recipe for neural cell survival or suicide

Farooqui

Horrocks

Farooqui

2007

J of Neuroscience Research

109

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The neural membranes contain phospholipids, sphingolipids, cholesterol, and proteins. Glycerophospholipids and sphingolipids are precursors for lipid mediators involved in signal transduction processes. Degradation of glycerophospholipids by phospholipase A(2) (PLA(2)) generates arachidonic acid (AA) and docosahexaenoic acids (DHA). Arachidonic acid is metabolized to eicosanoids and DHA is metabolized to docosanoids. The catabolism of glycosphingolipids generates ceramide, ceramide 1-phosphate, sphingosine, and sphingosine 1-phosphate. These metabolites modulate PLA(2) activity. Arachidonic acid, a product derived from glycerophospholipid catabolism by PLA(2), modulates sphingomyelinase (SMase), the enzyme that generates ceramide and phosphocholine. Furthermore, sphingosine 1-phosphate modulates cyclooxygenase, an enzyme responsible for eicosanoid production in brain. This suggests that an interplay and cross talk occurs between lipid mediators of glycerophospholipid and glycosphingolipid metabolism in brain tissue. This interplay between metabolites of glycerophospholipid and sphingolipid metabolism may play an important role in initiation and maintenance of oxidative stress associated with neurologic disorders as well as in neural cell proliferation, differentiation, and apoptosis. Recent studies indicate that PLA(2) and SMase inhibitors can be used as neuroprotective and anti-apoptotic agents. Development of novel inhibitors of PLA(2) and SMase may be useful for the treatment of oxidative stress, and apoptosis associated with neurologic disorders such as stroke, Alzheimer disease, Parkinson disease, and head and spinal cord injuries.

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2n-fatty acids from phosphatidylcholine label sphingolipids—A novel role of phospholipase A2?

Cited by 6 publications

References 44 publications

Aristolochic Acid Induced Suicidal Erythrocyte Death

Aristolochic Acid Induced Suicidal Erythrocyte Death

Evidence for inflammation-mediated memory dysfunction in gastropods: putative PLA2and COX inhibitors abolish long-term memory failure induced by systemic immune challenges

Interactions between neural membrane glycerophospholipid and sphingolipid mediators: A recipe for neural cell survival or suicide

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