ArticleThe American journal of pathology2003
Foreign body-type multinucleated giant cell formation is potently induced by alpha-tocopherol and prevented by the diacylglycerol kinase inhibitor R59022.
Article in The American journal of pathology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 69 citations in OpenAlex.
- Mechanisms of Foreign Body Giant Cell Formation in Response to Implantable Biomaterials.Polymers · 2023Review
- Roles of inflammatory cell infiltrate in periprosthetic osteolysis.Frontiers in immunology · 2023Review
- Device implant based on poly (lactic acid) with vitamin E for vaccine delivery system in Tilapia: Study for biocompatibility and biodegradation.Fish and shellfish immunology reports · 2022Article
- A microfluidic-based approach to investigate the inflammatory response of macrophages to pristine and drug-loaded nanostructured hydroxyapatite.Materials today. Bio · 2022Article
- Image-Based Evaluation of In Vivo Degradation for Shape-Memory Polymer Polyurethane Foam.Polymers · 2022Article
- Covalent linkage of sulfated hyaluronan to the collagen scaffold Mucograft® enhances scaffold stability and reduces proinflammatory macrophage activationBioactive materials · 2022Article
- Nanotopographical Coatings Induce an Early Phenotype-Specific Response of Primary Material-Resident M1 and M2 Macrophages.Materials (Basel, Switzerland) · 2020Article
- Sugar-based collagen membrane cross-linking increases barrier capacity of membranes.Clinical oral investigations · 2018Article
- A comparative multi-parametric in vitro model identifies the power of test conditions to predict the fibrotic tendency of a biomaterial.Scientific reports · 2017Article
- Associations between serum vitamin E concentration and bone mineral density in the US elderly population.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2017Article
- Bone Marrow Mesenchymal Stem Cell-Based Engineered Cartilage Ameliorates Polyglycolic Acid/Polylactic Acid Scaffold-Induced Inflammation Through M2 Polarization of Macrophages in a Pig Model.Stem cells translational medicine · 2016Article
- Phenotypic expression in human monocyte-derived interleukin-4-induced foreign body giant cells and macrophages in vitro: dependence on material surface properties.Journal of biomedical materials research. Part A · 2015Article
- Evaluation of long-term vitamin E insufficiency or excess on bone mass, density, and microarchitecture in rodents.Free radical biology & medicine · 2013Article
- Foreign body-type multinucleated giant cells induced by interleukin-4 express select lymphocyte co-stimulatory molecules and are phenotypically distinct from osteoclasts and dendritic cells.Experimental and molecular pathology · 2011Article
- Biocompatibility of implants: lymphocyte/macrophage interactions.Seminars in immunopathology · 2011Review
- Characterization of topographical effects on macrophage behavior in a foreign body response model.Biomaterials · 2010Article
- Macrophage fusion leading to foreign body giant cell formation persists under phagocytic stimulation by microspheres in vitro and in vivo in mouse models.Journal of biomedical materials research. Part A · 2010Article
- Vitronectin is a critical protein adhesion substrate for IL-4-induced foreign body giant cell formation.Journal of biomedical materials research. Part A · 2008Article
- Foreign body reaction to biomaterials.Seminars in immunology · 2008Review
- Foreign body-type multinucleated giant cell formation requires protein kinase C beta, delta, and zeta.Experimental and molecular pathology · 2008Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Multinucleated foreign body giant cells (FBGCs) form by monocyte-derived macrophage fusion on implanted biomedical devices and are believed to mediate oxidative damage to biomaterial surfaces. Our in vitro system of human macrophage culture and interleukin (IL)-4-induced FBGC formation was developed to study the macrophage fusion mechanism and the physiological significance of FBGCs on implanted biomaterials and at other sites of chronic inflammation. Here, we demonstrate that the antioxidant vitamin E (90% alpha-tocopherol) moderately induces macrophage fusion and increases IL-4-induced FBGC formation. Moreover, purified alpha-tocopherol, but not beta-, gamma-, or delta-tocopherol, most remarkably induces macrophage fusion, leading to cultures of confluent FBGCs below normal plasma concentrations. This is not observed with the similar antioxidants probucol or Trolox, suggesting that the alpha-tocopherol effects on FBGC formation are independent of its antioxidant activity. Consistent with the reported activation of diacylglycerol kinase by alpha-tocopherol, the diacylglycerol kinase inhibitor R59022 completely abrogates FBGC formation. R59022 inhibition of IL-4-induced FBGC formation is reversed by alpha-tocopherol, suggesting that FBGC formation involves diacylglycerol kinase activation. This study suggests a novel role for diacylglycerol kinase in the mechanism of macrophage fusion/FBGC formation at sites of chronic inflammation and reveals that the pleiotropic lipophilic compound, alpha-tocopherol, is a highly potent macrophage fusion factor.
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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 Socratic graph.