ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2011
Phospholipase A2 superfamily members play divergent roles after spinal cord injury.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 57 citations in OpenAlex.
- Arachidonic acid metabolism in spinal cord injury.Journal of advanced research · 2026Review
- sPLA2-IIA modifies progranulin deficiency phenotypes in mouse models.Molecular neurodegeneration · 2025Article
- Cytosolic phospholipase A2 in infiltrating monocyte derived macrophages does not impair recovery after spinal cord injury in female mice.Scientific reports · 2025Article
- Cytosolic Phospholipase A2 in Infiltrating Monocyte-Derived Macrophages Does Not Impair Recovery After Spinal Cord Injury in Female Mice.Research square · 2024Article
- Ferroptosis inhibitor improves outcome after early and delayed treatment in mild spinal cord injury.Acta neuropathologica · 2024Article
- Necroptosis pathway emerged as potential diagnosis markers in spinal cord injury.Journal of cellular and molecular medicine · 2024Article
- Article
- Chondroitin Sulfate Proteoglycans Revisited: Its Mechanism of Generation and Action for Spinal Cord Injury.Aging and disease · 2024Review
- iPLA2 inhibition blocks LysoPC-induced TRPC6 externalization and promotes Re-endothelialization of carotid injuries in hypercholesterolemic mice.Cell calcium · 2023Article
- Functions and mechanisms of cytosolic phospholipase ANeural regeneration research · 2023Review
- Drug screening in zebrafish larvae reveals inflammation-related modulators of secondary damage after spinal cord injury in mice.Theranostics · 2023Article
- Promising Advances in Pharmacotherapy for Patients with Spinal Cord Injury-A Review of Studies Performed In Vivo with Modern Drugs.Journal of clinical medicine · 2022Review
- Neutrophil, Extracellular Matrix Components, and Their Interlinked Action in Promoting Secondary Pathogenesis After Spinal Cord Injury.Molecular neurobiology · 2021Review
- The effects of myelin on macrophage activation are phenotypic specific via cPLAScientific reports · 2021Article
- RNA-seq analysis and compound screening highlight multiple signalling pathways regulating secondary cell death after acute CNS injuryBiology open · 2020Article
- Small-molecule inhibitors as potential therapeutics and as tools to understand the role of phospholipases ABiochimica et biophysica acta. Molecular and cell biology of lipids · 2019Review
- Article
- PLA2G6-Associated Neurodegeneration (PLAN): Review of Clinical Phenotypes and Genotypes.Frontiers in neurology · 2018Review
- Analyses of Calcium-Independent Phospholipase AMethods in enzymology · 2017Article
- Liberating Chiral Lipid Mediators, Inflammatory Enzymes, and LIPID MAPS from Biological Grease.The Journal of biological chemistry · 2016Review
Corrections and comments
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Authors and funding
14 authors at 6 institutions in 5 countries.
Funding
Abstract
Spinal cord injury (SCI) results in permanent loss of motor functions. A significant aspect of the tissue damage and functional loss may be preventable as it occurs, secondary to the trauma. We show that the phospholipase A(2) (PLA(2)) superfamily plays important roles in SCI. PLA(2) enzymes hydrolyze membrane glycerophospholipids to yield a free fatty acid and lysophospholipid. Some free fatty acids (arachidonic acid) give rise to eicosanoids that promote inflammation, while some lysophospholipids (lysophosphatidylcholine) cause demyelination. We show in a mouse model of SCI that two cytosolic forms [calcium-dependent PLA(2) group IVA (cPLA(2) GIVA) and calcium-independent PLA(2) group VIA (iPLA(2) GVIA)], and a secreted form [secreted PLA(2) group IIA (sPLA(2) GIIA)] are up-regulated. Using selective inhibitors and null mice, we show that these PLA(2)s play differing roles. cPLA(2) GIVA mediates protection, whereas sPLA(2) GIIA and, to a lesser extent, iPLA(2) GVIA are detrimental. Furthermore, completely blocking all three PLA(2)s worsens outcome, while the most beneficial effects are seen by partial inhibition of all three. The partial inhibitor enhances expression of cPLA(2) and mediates its beneficial effects via the prostaglandin EP1 receptor. These findings indicate that drugs that inhibit detrimental forms of PLA(2) (sPLA(2) and iPLA2) and up-regulate the protective form (cPLA2) may be useful for the treatment of SCI.
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Registered trials
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