ReviewJournal of molecular neuroscience : MN2000
Deacylation and reacylation of neural membrane glycerophospholipids.
Review in Journal of molecular neuroscience : MN, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 125 citations in OpenAlex.
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- Xanthoceraside Could Ameliorate Alzheimer's Disease Symptoms of Rats by Affecting the Gut Microbiota Composition and Modulating the Endogenous Metabolite Levels.Frontiers in pharmacology · 2019Article
- Plasma metabolomic biomarkers accurately classify acute mild traumatic brain injury from controls.PloS one · 2018Article
- Decreased 16:0/20:4-phosphatidylinositol level in the post-mortem prefrontal cortex of elderly patients with schizophrenia.Scientific reports · 2017Article
- Untargeted Metabolomics Reveals Intervention Effects of Total Turmeric Extract in a Rat Model of Nonalcoholic Fatty Liver Disease.Evidence-based complementary and alternative medicine : eCAM · 2016Article
- Docosahexaenoic (DHA) modulates phospholipid-hydroperoxide glutathione peroxidase (Gpx4) gene expression to ensure self-protection from oxidative damage in hippocampal cells.Frontiers in physiology · 2015Article
- The role of long chain fatty acids and their epoxide metabolites in nociceptive signaling.Prostaglandins & other lipid mediators · 2014Review
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- Chronic caloric restriction partially protects against age-related alteration in serum metabolome.Age (Dordrecht, Netherlands) · 2013Article
- Hormesis in aging and neurodegeneration-a prodigy awaiting dissection.International journal of molecular sciences · 2013Review
- Acetate supplementation attenuates lipopolysaccharide-induced neuroinflammation.Journal of neurochemistry · 2011Article
- Polyunsaturated fatty acids protect against prion-mediated synapse damage in vitro.Neurotoxicity research · 2010Article
- Cytosolic PLA2 is required for CTL-mediated immunopathology of celiac disease via NKG2D and IL-15.The Journal of experimental medicine · 2009Article
- Docosahexaenoic and eicosapentaenoic acids increase prion formation in neuronal cells.BMC biology · 2008Article
- Dietary n-3 PUFA deprivation alters expression of enzymes of the arachidonic and docosahexaenoic acid cascades in rat frontal cortex.Molecular psychiatry · 2007Article
- Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The deacylation-reacylation cycle is an important mechanism responsible for the introduction of polyunsaturated fatty acids into neural membrane glycerophospholipids. It involves four enzymes, namely acyl-CoA synthetase, acyl-CoA hydrolase, acyl-CoA: lysophospholipid acyltransferase, and phospholipase A2. All of these enzymes have been purified and characterized from brain tissue. Under normal conditions, the stimulation of neural membrane receptors by neurotransmitters and growth factors results in the release of arachidonic acid from neural membrane glycerophospholipids. The released arachidonic acid acts as a second messenger itself. It can be further metabolized to eicosanoids, a group of second messengers involved in a variety of neurochemical functions. A lysophospholipid, the second product of reactions catalyzed by phospholipase A2, is rapidly acylated with acyl-CoA, resulting in the maintenance of the normal and essential neural membrane glycerophospholipid composition. However, under pathological situations (ischemia), the overstimulation of phospholipase A2 results in a rapid generation and accumulation of free fatty acids including arachidonic acid, eicosanoids, and lipid peroxides. This results in neural inflammation, oxidative stress, and neurodegeneration. In neural membranes, the deacylation-reacylation cycle maintains a balance between free and esterified fatty acids, resulting in low levels of arachidonic acid and lysophospholipids. This is necessary for not only normal membrane integrity and function, but also for the optimal activity of the membrane-bound enzymes, receptors, and ion channels involved in normal signal-transduction processes.
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