ArticleThe Journal of biological chemistry2006
Calcium-independent phospholipase A2 localizes in and protects mitochondria during apoptotic induction by staurosporine.
Article in The Journal of biological chemistry, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.
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Who cites it
73 citing papers in PubMed, 126 citations in OpenAlex.
- Retromer-targeted therapy for neurodegenerative diseases.Molecular neurodegeneration · 2026Review
- Pla2g6 Deficiency Induces Neuronal Precursor Apoptosis During Neurodevelopment.International journal of molecular sciences · 2026Article
- Decanoic acid extends lifespan and modulates metabolism in models of PLA2G6-associated neurodegeneration.Disease models & mechanisms · 2025Article
- Endoplasmic reticulum stress and mitochondrial dysfunction during aging: Role of sphingolipids.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2023Article
- Mitochondrial HAnnual review of physiology · 2022Review
- iPLACells · 2021Article
- The Role of Oxidative Stress in Pancreatic β Cell Dysfunction in Diabetes.International journal of molecular sciences · 2021Review
- iPLA2-VIA is required for healthy aging of neurons, muscle, and the female germline in Drosophila melanogaster.PloS one · 2021Article
- Mitochondrial Dysfunction, Oxidative Stress and Neuroinflammation in Neurodegeneration with Brain Iron Accumulation (NBIA).Antioxidants (Basel, Switzerland) · 2020Review
- Substantia nigra echogenicity is associated with serum ferritin, gender and iron-related genes in Parkinson's disease.Scientific reports · 2020Article
- iPLABiochimica et biophysica acta. Molecular and cell biology of lipids · 2019Review
- Current perspective of mitochondrial biology in Parkinson's disease.Neurochemistry international · 2018Review
- Infantile Neuroaxonal Dystrophy: Diagnosis and Possible Treatments.Frontiers in genetics · 2018Article
- Coenzyme Q10 suppresses apoptosis of mouse pancreatic β-cell line MIN6.Diabetology & metabolic syndrome · 2018Article
- Article
- Mitochondria: A Common Target for Genetic Mutations and Environmental Toxicants in Parkinson's Disease.Frontiers in genetics · 2017Review
- Cardiolipin remodeling: a regulatory hub for modulating cardiolipin metabolism and function.Journal of bioenergetics and biomembranes · 2016Review
- Mitochondrial phospholipids: role in mitochondrial function.Journal of bioenergetics and biomembranes · 2016Review
- Review: Insights into molecular mechanisms of disease in neurodegeneration with brain iron accumulation: unifying theories.Neuropathology and applied neurobiology · 2016Review
- Disruption of Golgi morphology and altered protein glycosylation in PLA2G6-associated neurodegeneration.Journal of medical genetics · 2016Article
13 more citing papers are in PubMed but not listed here.
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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Mitochondria-mediated production of reactive oxygen species (ROS) plays a key role in apoptosis. Mitochondrial phospholipid cardiolipin molecules are likely the main target of ROS because they are particularly rich in polyunsaturated fatty acids. They are also located in the inner mitochondrial membrane near the ROS-producing sites. Under physiological conditions mitochondria can repair peroxidative damage in part through a remodeling mechanism via the deacylation-reacylation cycle mediated by phospholipase A2 (PLA2) and acyl-coenzyme A-dependent monolysocardiolipin acyltransferase. Here we investigate whether group VIA Ca2+-independent PLA2 (iPLA2) plays a role in the protection of mitochondrial function from damage caused by mitochondrially generated ROS during apoptotic induction by staurosporine (STS). We show that iPLA2-expressing cells were relatively resistant to STS-induced apoptosis. iPLA2 localized to mitochondria even before apoptotic induction, and most iPLA2-associated mitochondria were intact in apoptotic resistant cells. Expression of iPLA2 in INS-1 cells prevented the loss of mitochondrial membrane potential, attenuated the release of cytochrome c, Smac/DIABLO, and apoptosis inducing factor from mitochondria, and reduced mitochondrial reactive oxygen species production. Inhibition of caspase 8 has little effect on STS-induced apoptosis in INS-1 cells. Finally, we found that STS down-regulated endogenous iPLA2 transcription in both INS-1 and iPLA2-expressing INS-1 cells without affecting the expression of group IV Ca2+-dependent PLA2. Together, our data indicate that iPLA2 is important for the protection of mitochondrial function from oxidative damage during apoptotic induction. Down-regulation of endogenous iPLA2 by STS may result in the loss of mitochondrial membrane repair functions and lead to mitochondrial failure and apoptosis.
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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.