ArticleCell biochemistry and biophysics2011
LPS-induced formation of immunoproteasomes: TNF-α and nitric oxide production are regulated by altered composition of proteasome-active sites.
Article in Cell biochemistry and biophysics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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46 citing papers in PubMed, 66 citations in OpenAlex.
- Emerging role of the immunoproteasome as a druggable target in lung inflammatory diseases.Respiratory research · 2026Review
- Multifaceted regulation of thymic tolerance by pattern recognition cascades.Frontiers in immunology · 2026Review
- Cleaving Expectations: A Review of Proteasome Functional and Catalytic Diversity.Biomolecules · 2025Review
- Review
- Tungsten disulfide atomic crystals with RONS scavenging and liver targeting capabilities for acetaminophen-induced acute liver injury therapy.Journal of nanobiotechnology · 2025Article
- Current landscape of the immunoproteasome: implications for disease and therapy.Cell death discovery · 2025Review
- Lung immune incompetency after mild peritoneal sepsis and its partial restoration by type 1 interferon: a mouse model study.Intensive care medicine experimental · 2024Article
- iRhom2 deficiency reduces sepsis-induced mortality associated with the attenuation of lung macrophages in mice.Histochemistry and cell biology · 2024Article
- Immunoproteasomal Inhibition With ONX-0914 Attenuates Atherosclerosis and Reduces White Adipose Tissue Mass and Metabolic Syndrome in Mice.Arteriosclerosis, thrombosis, and vascular biology · 2024Article
- 2,4'-Dihydroxybenzophenone: A Promising Anti-Inflammatory Agent Targeting Toll-like Receptor 4/Myeloid Differentiation Factor 2-Mediated Mitochondrial Reactive Oxygen Species Production during Lipopolysaccharide-Induced Systemic Inflammation.ACS pharmacology & translational science · 2024Article
- Synergistic modulation of proinflammatory mediators and cytokines in lipopolysaccharide-activated RAW 264.7 macrophages: The therapeutic potential ofVeterinary world · 2024Article
- The Coding Logic of Interoception.Annual review of physiology · 2024Review
- Less Severe Polymicrobial Sepsis in ConditionalInternational journal of molecular sciences · 2023Article
- Dysregulation of Gene Expression of Key Signaling Mediators in PBMCs from People with Type 2 Diabetes Mellitus.International journal of molecular sciences · 2023Article
- Low-level Cu-fortification of bovine lactoferrin: Focus on its effect on in vitro anti-inflammatory activity in LPS-stimulated macrophages.Current research in food science · 2023Article
- A Novel Mechanism of Immunoproteasome Regulation via miR-369-3p in Intestinal Inflammatory Response.International journal of molecular sciences · 2022Article
- Reprograming of Gene Expression of Key Inflammatory Signaling Pathways in Human Peripheral Blood Mononuclear Cells by Soybean Lectin and Resveratrol.International journal of molecular sciences · 2022Article
- The Relationship between the M1/M2 Macrophage Polarization and the Degree of Ossicular Erosion in Human Acquired Cholesteatoma: An Immunohistochemical Study.Journal of clinical medicine · 2022Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Stimulation of mouse macrophages with LPS leads to tumor necrosis factor (TNF-α) secretion and nitric oxide (NO) release at different times through independent signaling pathways. While the precise regulatory mechanisms responsible for these distinct phenotypic responses have not been fully delineated, results of our recent studies strongly implicate the cellular cytoplasmic ubiquitin-proteasome pathway as a key regulator of LPS-induced macrophage inflammatory responses. Our objective in this study was to define the relative contribution of specific proteasomal active-sites in induction of TNF-α and NO after LPS treatment of RAW 264.7 macrophages using selective inhibitors of these active sites. Our data provide evidence that LPS stimulation of mouse macrophages triggers a selective increase in the levels of gene and protein expression of the immunoproteasomes, resulting in a modulation of specific functional activities of the proteasome and a corresponding increase in NO production as compared to untreated controls. These findings suggest the LPS-dependent induction of immunoproteasome. In contrast, we also demonstrate that TNF-α expression is primarily dependent on both the chymotrypsin- and the trypsin-like activities of X, Y, Z subunits of the proteasome. Proteasome-associated post-acidic activity alone also contributes to LPS-induced expression of TNF-α. Taken together; our results indicate that LPS-induced TNF-α in macrophages is differentially regulated by each of the three proteasome activities. Since addition of proteasome inhibitors to mouse macrophages profoundly affects the degradation of proteins involved in signal transduction, we conclude that proteasome-specific degradation of several signaling proteins is likely involved in differential regulation of LPS-dependent secretion of proinflammatory mediators.
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