1. Acute catabolism of leukocyte lipid bodies: Characterization of a nordihydroguaiaretic acid (NDGA)-induced proteasomal-dependent model.
- Author
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de Lira MN, Bolini L, Amorim NRT, Silva-Souza HA, Diaz BL, Canetti C, Persechini PM, and Bandeira-Melo C
- Subjects
- Animals, Eosinophils drug effects, Eosinophils metabolism, Leukocytes metabolism, Lipid Droplets metabolism, Macrophages drug effects, Macrophages metabolism, Mice, Neutrophils drug effects, Neutrophils metabolism, Proteasome Endopeptidase Complex metabolism, Leukocytes drug effects, Lipid Droplets drug effects, Lipoxygenase Inhibitors pharmacology, Masoprocol pharmacology, Proteasome Endopeptidase Complex drug effects
- Abstract
Cytoplasmic availability of leukocyte lipid bodies is controlled by a highly regulated cycle of opposing biogenesis- and catabolism-related events. While leukocyte biogenic machinery is well-characterized, lipid body catabolic mechanisms are yet mostly unknown. Here, we demonstrated that nordihydroguaiaretic acid (NDGA) very rapidly decreases the numbers of pre-formed lipid bodies within lipid body-enriched cytoplasm of mouse leukocytes - macrophages, neutrophils and eosinophils. NDGA mechanisms driving leukocyte lipid body disappearance were not related to loss of cell viability, 5-lipoxygenase inhibition, ATP autocrine/paracrine activity, or biogenesis inhibition. Proteasomal-dependent breakdown of lipid bodies appears to control NDGA-driven leukocyte lipid body reduction, since it was Bortezomib-sensitive in macrophages, neutrophils and eosinophils. Our findings unveil an acute NDGA-triggered lipid body catabolic event - a novel experimental model for the still neglected research area on leukocyte lipid body catabolism, additionally favoring further insights on proteasomal contribution to lipid body breakdown., (Copyright © 2021 Elsevier Ltd. All rights reserved.)
- Published
- 2021
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