ArticleThe Journal of biological chemistry2009
Suppression of mitochondrial function by oxidatively truncated phospholipids is reversible, aided by bid, and suppressed by Bcl-XL.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
22 citing papers in PubMed, 41 citations in OpenAlex.
- APOE modulates microglial immunometabolism in response to age, amyloid pathology, and inflammatory challenge.Cell reports · 2023Article
- Mitochondrial Lipids: From Membrane Organization to Apoptotic Facilitation.International journal of molecular sciences · 2022Review
- Conformational States of the Cytoprotective Protein Bcl-xL.Biophysical journal · 2020Article
- Redox Epiphospholipidome in Programmed Cell Death Signaling: Catalytic Mechanisms and Regulation.Frontiers in endocrinology · 2020Review
- Lipoprotein Particle Formation by Proapoptotic tBid.Biophysical journal · 2018Article
- Frontiers of Complex Disease Mechanisms: Membrane Surface Tension May Link Genotype to Phenotype in Glaucoma.Frontiers in cell and developmental biology · 2018Article
- Mitochondrial outer membrane permeabilization: a focus on the role of mitochondrial membrane structural organization.Biophysical reviews · 2017Review
- Serum Dyslipidemia Is Induced by Internal Exposure to Strontium-90 in Mice, Lipidomic Profiling Using a Data-Independent Liquid Chromatography-Mass Spectrometry Approach.Journal of proteome research · 2015Article
- Inflammatory PAF Receptor Signaling Initiates Hedgehog Signaling and Kidney Fibrogenesis During Ethanol Consumption.PloS one · 2015Article
- Lipid peroxidation generates biologically active phospholipids including oxidatively N-modified phospholipids.Chemistry and physics of lipids · 2014Review
- Membrane changes under oxidative stress: the impact of oxidized lipids.Biophysical reviews · 2014Review
- Bioactive lipids-based pH sensitive micelles for co-delivery of doxorubicin and ceramide to overcome multidrug resistance in leukemia.Pharmaceutical research · 2013Article
- Circulating biologically active oxidized phospholipids show on-going and increased oxidative stress in older male mice.Redox biology · 2013Article
- Metabolic signature of electrosurgical liver dissection.PloS one · 2013Article
- Bioactive oxidatively truncated phospholipids in inflammation and apoptosis: formation, targets, and inactivation.Biochimica et biophysica acta · 2012Review
- Oxidized phosphatidylcholines promote phase separation of cholesterol-sphingomyelin domains.Biophysical journal · 2012Article
- Acetaminophen inhibits cytochrome c redox cycling induced lipid peroxidation.Biochemical and biophysical research communications · 2012Article
- Oxidatively truncated phospholipids are required agents of tumor necrosis factor α (TNFα)-induced apoptosis.The Journal of biological chemistry · 2012Article
- Bcl-xL enhances single-cell survival and expansion of human embryonic stem cells without affecting self-renewal.Stem cell research · 2012Article
- Oxidized phosphatidylcholines facilitate phospholipid flip-flop in liposomes.Biophysical journal · 2011Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Oxidatively truncated phospholipids are present in atherosclerotic lesions, apoptotic cells, and oxidized low density lipoproteins. Some of these lipids rapidly enter cells to induce apoptosis by the intrinsic pathway, but how such lipids initiate this process is unknown. We show the truncated phospholipid hexadecyl azelaoyl glycerophosphocholine (Az-LPAF), derived from the fragmentation of abundant sn-2 linoleoyl residues, depolarized mitochondria of intact cells. Az-LPAF also depolarized isolated mitochondria and allowed NADH loss, but did not directly interfere with complex I function. Cyclosporin A blockade of the mitochondrial permeability transition pore partially prevented the loss of electrochemical potential. Depolarization of isolated mitochondria by the truncated phospholipid was readily reversed by the addition of albumin that sequestered this lipid. Ectopic expression of the anti-apoptotic protein Bcl-X(L) in HL-60 cells reduced apoptosis by the truncated phospholipid by protecting their mitochondria. Mitochondria isolated from these cells were also protected from Az-LPAF-induced depolarization. Conversely mitochondria isolated from Bid(-/-) animals that lack this pro-apoptotic Bcl-2 family member were resistant to Az-LPAF depolarization. Addition of recombinant full-length Bid, which has phospholipid transfer activity, restored this sensitivity. Thus, phospholipid oxidation products physically interact with mitochondria to continually depolarize this organelle without permanent harm, and Bcl-2 family members modulate this interaction with full-length Bid acting as a co-factor for pro-apoptotic, oxidatively truncated phospholipids.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.