ArticleScientific reports2014
Resistance of LPS-activated bone marrow derived macrophages to apoptosis mediated by dexamethasone.
Article in Scientific reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- Article
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- Dexmedetomidine attenuates inflammation and organ injury partially by upregulating Nur77 in sepsis.Immunity, inflammation and disease · 2023Article
- The Use of Acute Immunosuppressive Therapy to Improve Antibiotic Efficacy against Intracellular Staphylococcus aureus.Microbiology spectrum · 2022Article
- Glucocorticoid Receptor β Isoform Predominates in the Human Dysplastic Brain Region and Is Modulated by Age, Sex, and Antiseizure Medication.International journal of molecular sciences · 2022Article
- Glucocorticoid Receptor β (GRβ): Beyond Its Dominant-Negative Function.International journal of molecular sciences · 2021Review
- From "Leaky Gut" to Impaired Glia-Neuron Communication in Depression.Advances in experimental medicine and biology · 2021Article
- Disease-Triggered Drug Release Effectively Prevents Acute Inflammatory Flare-Ups, Achieving Reduced Dosing.Small (Weinheim an der Bergstrasse, Germany) · 2018Article
- Microglial Activation Results in Inhibition of TGF-β-Regulated Gene Expression.Journal of molecular neuroscience : MN · 2017Article
- High-dose dexamethasone induced LPS-stimulated rat alveolar macrophages apoptosis.Drug design, development and therapy · 2017Article
- LPS regulates the expression of glucocorticoid receptor α and β isoforms and induces a selective glucocorticoid resistance in vitro.Journal of inflammation (London, England) · 2017Article
- Unexpected cellular players in Rett syndrome pathology.Neurobiology of disease · 2016Review
- Mapping the pulmonary environment of animals protected from virulent H1N1 influenza infection using the TLR-2 agonist Pam₂Cys.Immunology and cell biology · 2016Article
- Endothelial Response to Glucocorticoids in Inflammatory Diseases.Frontiers in immunology · 2016Review
- Ginseng alleviates cyclophosphamide-induced hepatotoxicity via reversing disordered homeostasis of glutathione and bile acid.Scientific reports · 2015Article
- Direct chemotherapeutic dual drug delivery through intra-articular injection for synergistic enhancement of rheumatoid arthritis treatment.Scientific reports · 2015Article
- Loss of the endothelial glucocorticoid receptor prevents the therapeutic protection afforded by dexamethasone after LPS.PloS one · 2014Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glucocorticoids (GC) display pleiotropic effects on the immune system. Macrophages are a major target for GC action. Here we show that dexamethasone (DEX), a synthetic GC, decreased viability of naïve bone marrow-derived macrophages (BMDM), involving an apoptotic mechanism. Administration of DEX together with lipopolysaccharide (LPS) protected BMDM against DEX-mediated cell death, suggesting that activated BMDM respond to DEX differently than naïve BMDM. An insight to the molecular basis of LPS actions was provided by a 7 fold increase in mRNA levels of glucocorticoid receptor beta (GRβ), a GR dominant-negative splice variant which inhibits GRα's transcriptional activity. LPS did not inhibit all DEX-mediated effects on BMDM; DEX significantly reduced the percentage of BMDM expressing high levels of the cell surface markers F4/80 and CD11b and led to a decrease in macrophage inflammatory protein 1 alpha (MIP1-α) mRNA and protein levels. These two DEX-mediated effects were not prevented by LPS. Our finding that LPS did not reduce the DEX-induced elevation of glucocorticoid-induced leucine zipper (GILZ), a mediator of GCs anti-inflammatory actions, may provide an underlying mechanism. These findings enable a better understanding of clinical states, such as sepsis, in which macrophages are activated by endotoxins and treatment by GCs is considered.
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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.