ArticleArthritis & rheumatology (Hoboken, N.J.)2016
Inhibition of G Protein βγ Subunit Signaling Abrogates Nephritis in Lupus-Prone Mice.
Article in Arthritis & rheumatology (Hoboken, N.J.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 13 citations in OpenAlex.
- Gallein-Loaded Albumin Nanoparticles Prevent Amyloid-β-Induced Amyloidogenic APP Processing, Synaptic Loss, and Dendritic Pathology.Molecular neurobiology · 2026Article
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- Biasing G protein βγ subunit downstream signaling enhances the analgesic effects of endogenous opioid receptor agonists during nitroglycerin-induced thermal hypersensitivity.Molecular pharmacology · 2025Article
- Biasing GMolecular pharmacology · 2024Article
- Gene Expression Profiles in Primary Sjögren's Syndrome With and Without Systemic Manifestations.ACR open rheumatology · 2019Article
- Article
- Novel Autoantibodies Related to Cell Death and DNA Repair Pathways in Systemic Lupus Erythematosus.Genomics, proteomics & bioinformatics · 2019Article
- Targeting G protein-coupled receptor signalling by blocking G proteins.Nature reviews. Drug discovery · 2018Review
- Gallein, a Gβγ subunit signalling inhibitor, inhibits metastatic spread of tumour cells expressing OR51E2 and exposed to its odorant ligand.BMC research notes · 2017Article
- PKK deficiency in B cells prevents lupus development in Sle lupus mice.Immunology letters · 2017Article
- Regulation of Chemokine Signal Integration by Activator of G-Protein Signaling 4 (AGS4).The Journal of pharmacology and experimental therapeutics · 2017Article
- Sex-specific effects of LiCl treatment on preservation of renal function and extended life-span in murine models of SLE: perspective on insights into the potential basis for survivorship in NZB/W female mice.Biology of sex differences · 2016Review
- Mechanisms for enhancement of μ-opioid receptor-mediated antinociception in the central nervous system through gallein-dependent modulation of downstream G protein βγ subunit signaling.Molecular pharmacologyArticle
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
objectiveDespite considerable advances in the understanding of systemic lupus erythematosus (SLE), there is still an urgent need for new and more targeted treatment approaches. We previously demonstrated that small-molecule blockade of G protein βγ subunit (Gβγ) signaling inhibits acute inflammation through inhibition of chemokine receptor signal transduction. We undertook this study to determine whether inhibition of Gβγ signaling ameliorates disease in a mouse model of SLE.
methodsLupus-prone (NZB × NZW)F1 female mice were prophylactically or therapeutically treated with the small-molecule Gβγ inhibitor gallein. Tissue samples were analyzed by flow cytometry and immunohistochemistry. The development and extent of nephritis were assessed by monitoring proteinuria and by immunohistochemical analysis. Serum immunoglobulin levels were measured by enzyme-linked immunosorbent assay, and total IgG and anti-double-stranded DNA (anti-dsDNA) antibody-secreting cells were measured by enzyme-linked immunospot assay.
resultsGallein inhibited accumulation of T cells and germinal center (GC) B cells in the spleen. Both prophylactic and therapeutic treatment reduced GC size, decreased antibody-secreting cell production in the spleen, and markedly decreased accumulation of autoreactive anti-dsDNA antibody-secreting cells in kidneys. Gallein also reduced immune complex deposition in kidneys. Finally, gallein treatment dramatically inhibited kidney inflammation, prevented glomerular damage, and decreased proteinuria. Mechanistically, gallein inhibited immune cell migration and signaling in response to chemokines in vitro, which suggests that its mechanisms of action in vivo are inhibition of migration of immune cells to sites of inflammation and inhibition of immune cell maturation.
conclusionOverall, these data demonstrate the potential use of gallein or novel inhibitors of Gβγ signaling in SLE treatment.
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