MG-132 interferes with iron cellular homeostasis and alters virulence of bovine herpesvirus 1
| Autor: | Luisa De Martino, Gian Carlo Tenore, Roberto Ciampaglia, Francesca Paola Nocera, Maria Grazia Ferraro, Carlo Irace, Filomena Fiorito, Rita Santamaria, Marialuisa Piccolo |
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| Přispěvatelé: | Fiorito, F, Irace, C, Nocera, Fp, Piccolo, M, Ferraro, Mg, Ciampaglia, R, Tenore, Gc, Santamaria, R, De Martino, L. |
| Rok vydání: | 2021 |
| Předmět: |
Programmed cell death
Leupeptins 040301 veterinary sciences Cellular homeostasis Transferrin receptor Virus Replication Cell Line 0403 veterinary science 03 medical and health sciences chemistry.chemical_compound Western blot medicine Animals Homeostasis Herpesvirus 1 Bovine 030304 developmental biology 0303 health sciences Virulence General Veterinary biology medicine.diagnostic_test Chemistry Acridine orange 04 agricultural and veterinary sciences biology.organism_classification Bovine herpesvirus 1 Cell biology Ferritin Proteasome inhibitor biology.protein Cattle medicine.drug |
| Zdroj: | Research in Veterinary Science. 137:1-8 |
| ISSN: | 0034-5288 |
| DOI: | 10.1016/j.rvsc.2021.04.023 |
| Popis: | Bovine herpesvirus 1 (BoHV-1) requires an iron-replete cell host to replicate efficiently. BoHV-1 infection provokes an increase in ferritin levels and a decrease of transferrin receptor 1 (TfR-1) expression, ultimately lowering iron pool extent. Thus, cells try to limit iron availability for virus spread. It has been demonstrated that MG-132, a proteasome inhibitor, reduces BoHV-1 release. Since ferritin, the major iron storage protein in mammalian cells, undergoes proteasome-mediated degradation, herein, the influence of MG-132 on iron metabolism during BoHV-1 infection was examined. Following infection in bovine cells (MDBK), MG-132 reduced cell death and viral yield. Western blot analysis showed a significant ferritin accumulation, likely due to the inhibition of its proteasome-mediated degradation pathway. In addition, the concomitant down-regulation of TfR-1 expression, observed during infection, was counteracted by proteasome inhibitor. This trend may be explained by enhanced acidic vesicular organelles, detected by acridine orange staining, determining a reduction of intracellular pH, that promotes new synthesis of TfR-1 degraded in a recycling pathway. In addition, MG-132 influences cellular iron distribution during BoHV-1 infection, as revealed by Perls' Prussian blue staining. However, cellular iron content, evaluated by Atomic Absorption Spectrophotometry, resulted essentially unaltered. These findings reveal that MG-132 may contribute to limit cellular iron availability for virus replication thereby enhancing cell survival. |
| Databáze: | OpenAIRE |
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