ArticleAmerican journal of physiology. Lung cellular and molecular physiology2016
Biosynthesis of oxidized lipid mediators via lipoprotein-associated phospholipase A2 hydrolysis of extracellular cardiolipin induces endothelial toxicity.
Article in American journal of physiology. Lung cellular and molecular physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- Alterations of Bioactive Lipid Profiles in the Retina Following Traumatic Optic Neuropathy in Mice.Biomolecules · 2025Article
- Mitophagy in atherosclerosis: from mechanism to therapy.Frontiers in immunology · 2023Review
- Article
- Mitochondrial dysfunction in vascular endothelial cells and its role in atherosclerosis.Frontiers in physiology · 2022Review
- Current Knowledge on the Role of Cardiolipin Remodeling in the Context of Lipid Oxidation and Barth Syndrome.Frontiers in molecular biosciences · 2022Article
- iPLA2β-mediated lipid detoxification controls p53-driven ferroptosis independent of GPX4.Nature communications · 2021Article
- Mitochondrial DAMPs and altered mitochondrial dynamics in OxLDL burden in atherosclerosis.Molecular and cellular biochemistry · 2021Review
- Oxidized Phospholipids in Control of Endothelial Barrier Function: Mechanisms and Implication in Lung Injury.Frontiers in endocrinology · 2021Review
- Outer Membrane Lipid Secretion and the Innate Immune Response to Gram-Negative Bacteria.Infection and immunity · 2020Review
- Lipoprotein-associated phospholipase A2: The story continues.Medicinal research reviews · 2020Review
- Redox (phospho)lipidomics of signaling in inflammation and programmed cell death.Journal of leukocyte biology · 2019Review
- "Redox lipidomics technology: Looking for a needle in a haystack".Chemistry and physics of lipids · 2019Review
- Disentangling oxidation/hydrolysis reactions of brain mitochondrial cardiolipins in pathogenesis of traumatic injury.JCI insight · 2018Article
- Lipid mediators in the regulation of endothelial barriers.Tissue barriers · 2018Review
- Oxidative lipidomics: applications in critical care.Current opinion in critical care · 2017Review
- The phospholipase iPLAThe Journal of biological chemistry · 2017Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
We (66) have previously described an NSAID-insensitive intramitochondrial biosynthetic pathway involving oxidation of the polyunsaturated mitochondrial phospholipid, cardiolipin (CL), followed by hydrolysis [by calcium-independent mitochondrial calcium-independent phospholipase A2-γ (iPLA2γ)] of oxidized CL (CLox), leading to the formation of lysoCL and oxygenated octadecadienoic metabolites. We now describe a model system utilizing oxidative lipidomics/mass spectrometry and bioassays on cultured bovine pulmonary artery endothelial cells (BPAECs) to assess the impact of CLox that we show, in vivo, can be released to the extracellular space and may be hydrolyzed by lipoprotein-associated PLA2 (Lp-PLA2). Chemically oxidized liposomes containing bovine heart CL produced multiple oxygenated species. Addition of Lp-PLA2 hydrolyzed CLox and produced (oxygenated) monolysoCL and dilysoCL and oxidized octadecadienoic metabolites including 9- and 13-hydroxyoctadecadienoic (HODE) acids. CLox caused BPAEC necrosis that was exacerbated by Lp-PLA2 Lower doses of nonlethal CLox increased permeability of BPAEC monolayers. This effect was exacerbated by Lp-PLA2 and partially mimicked by authentic monolysoCL or 9- or 13-HODE. Control mice plasma contained virtually no detectable CLox; in contrast, 4 h after Pseudomonas aeruginosa (P. aeruginosa) infection, 34 ± 8 mol% (n = 6; P < 0.02) of circulating CL was oxidized. In addition, molar percentage of monolysoCL increased twofold after P. aeruginosa in a subgroup analyzed for these changes. Collectively, these studies suggest an important role for 1) oxidation of CL in proinflammatory environments and 2) possible hydrolysis of CLox in extracellular spaces producing lysoCL and oxidized octadecadienoic acid metabolites that may lead to impairment of pulmonary endothelial barrier function and necrosis.
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