ArticleArteriosclerosis, thrombosis, and vascular biology2014
Group VIA phospholipase A2 mediates enhanced macrophage migration in diabetes mellitus by increasing expression of nicotinamide adenine dinucleotide phosphate oxidase 4.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 21 citations in OpenAlex.
- Nox4 as a novel therapeutic target for diabetic vascular complications.Redox biology · 2023Review
- Noncanonical Regulation of cAMP-Dependent Insulin Secretion and Its Implications in Type 2 Diabetes.Comprehensive Physiology · 2023Article
- Nox4 expression in osteo-progenitors controls bone development in mice during early life.Communications biology · 2022Article
- [Role of p22phox and NOX5 in autophagy and apoptosis of osteoblasts induced by hypoxia].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2021Article
- The Impact of the CaBiomolecules · 2021Review
- Metabolic Effects of Selective Deletion of Group VIA Phospholipase ABiomolecules · 2020Article
- Article
- Nox4 Expression Is Not Required for OVX-Induced Osteoblast Senescence and Bone Loss in Mice.JBMR plus · 2020Article
- Macrophage polarization is linked to CaJournal of lipid research · 2020Article
- iPLABiochimica et biophysica acta. Molecular and cell biology of lipids · 2019Review
- Polarization of Macrophages toward M2 Phenotype Is Favored by Reduction in iPLA2β (Group VIA Phospholipase A2).The Journal of biological chemistry · 2016Article
- Mice with Genetic Deletion of Group VIA Phospholipase A2β Exhibit Impaired Macrophage Function and Increased Parasite Load in Trypanosoma cruzi-Induced Myocarditis.Infection and immunity · 2016Article
- Calcium-independent phospholipases A2 and their roles in biological processes and diseases.Journal of lipid research · 2015Review
- Definition of a Novel Pathway Centered on Lysophosphatidic Acid To Recruit Monocytes during the Resolution Phase of Tissue Inflammation.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- p47phox-Nox2-dependent ROS Signaling Inhibits Early Bone Development in Mice but Protects against Skeletal Aging.The Journal of biological chemistry · 2015Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
objectiveWe previously demonstrated that nicotinamide adenine dinucleotide phosphate oxidase 4 (Nox4) mediates increased monocyte priming and chemotaxis under conditions of diabetic metabolic stress, and emerging data indicate that group VIA phospholipase A2 (iPLA2β) also participates in regulating monocyte chemotaxis. Here, we examined relationships between iPLA2β expression and Nox4 action in mouse peritoneal macrophages subjected to diabetic metabolic stress. APPROACH AND
resultsIncreased iPLA2β expression and activity were observed in macrophages from low-density lipoprotein receptor knockout mice that were fed a high-fat diet, and this was associated with time-dependent increases in atherosclerotic lesion size and macrophage content. Incubating macrophages with 30 mmol/L D-glucose, 100 μg/mL low-density lipoprotein, or both (D-glucose+low-density lipoprotein) induced a robust increase in iPLA2β expression and activity and in cell migration in response to monocyte chemoattractant protein-1. The increases in iPLA2β activity and cell migration were prevented by a bromoenol lactone iPLA2β suicide inhibitor or an iPLA2β antisense oligonucleotide. Incubating macrophages under conditions that mimic diabetic metabolic stress ex vivo resulted in increased Nox4 expression and activity and hydrogen peroxide generation compared with controls. Bromoenol lactone prevented those effects without affecting Nox2 expression. Nox4 inhibition eliminated diabetic metabolic stress-induced acceleration of macrophage migration. Lysophosphatidic acid restored Nox4 expression, hydrogen peroxide generation, and migration to bromoenol lactone-treated cells, and a lysophosphatidic acid receptor antagonist abrogated iPLA2β-mediated increases in Nox4 expression.
conclusionsTaken together, these observations identify iPLA2β and lysophosphatidic acid derived from its action as critical in regulating macrophage Nox4 activity and migration in the diabetic state in vivo and under similar conditions ex vivo.
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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 OpenQuestion graph.