ArticleArthritis and rheumatism2010
Bim-Bcl-2 homology 3 mimetic therapy is effective at suppressing inflammatory arthritis through the activation of myeloid cell apoptosis.
Article in Arthritis and rheumatism, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
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Who cites it
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.
- Cationic Arginine-Rich Peptides (CARPs): A Novel Class of Neuroprotective Agents With a Multimodal Mechanism of Action.Frontiers in neurology · 2020Pooled it
- Induction of caspase-mediated suppression of interferon signaling potentiates viral oncolysis of resistant tumor cells.Cell communication and signaling : CCS · 2026Article
- Targeting the BCL2 Family: Advances and Challenges in BH3 Mimetic-Based Therapies.International journal of molecular sciences · 2025Review
- Dying to Defend: Neutrophil Death Pathways and their Implications in Immunity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Review
- Apoptotic cell death in disease-Current understanding of the NCCD 2023.Cell death and differentiation · 2023Review
- Bim Expression Promotes the Clearance of Mononuclear Phagocytes during Choroidal Neovascularization, Mitigating Scar Formation in Mice.Life (Basel, Switzerland) · 2022Article
- Targeting RIP Kinases in Chronic Inflammatory Disease.Biomolecules · 2021Review
- BAD inactivation exacerbates rheumatoid arthritis pathology by promoting survival of sublining macrophages.eLife · 2020Article
- Article
- Review
- The Role of Macrophages in the Response to TNF Inhibition in Experimental Arthritis.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Bim suppresses the development of SLE by limiting myeloid inflammatory responses.The Journal of experimental medicine · 2017Article
- The contribution of the programmed cell death machinery in innate immune cells to lupus nephritis.Clinical immunology (Orlando, Fla.) · 2017Review
- The caspase-8/RIPK3 signaling axis in antigen presenting cells controls the inflammatory arthritic response.Arthritis research & therapy · 2017Article
- The inflammatory role of phagocyte apoptotic pathways in rheumatic diseases.Nature reviews. Rheumatology · 2016Review
- ApoE deficiency exacerbates the development and sustainment of a semi-chronic K/BxN serum transfer-induced arthritis model.Journal of translational medicine · 2016Article
- Regulation of Bim in Health and Disease.Oncotarget · 2015Review
- Reactivity of rat bone marrow-derived macrophages to neurotransmitter stimulation in the context of collagen II-induced arthritis.Arthritis research & therapy · 2015Article
- The Interplay Between Monocytes/Macrophages and CD4(+) T Cell Subsets in Rheumatoid Arthritis.Frontiers in immunology · 2015Review
- Sympathetic Neurotransmitters Modulate Osteoclastogenesis and Osteoclast Activity in the Context of Collagen-Induced Arthritis.PloS one · 2015Article
Corrections and comments
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Authors and funding
12 authors at 7 institutions in 2 countries.
Funding
Abstract
objectiveRheumatoid arthritis (RA) is a destructive autoimmune disease characterized by an increased inflammation in the joint. Therapies that activate the apoptotic cascade may have potential for use in RA; however, few therapeutic agents fit this category. The purpose of this study was to examine the potential of Bim, an agent that mimics the action of Bcl-2 homology 3 (BH3) domain-only proteins that have shown success in preclinical studies of cancer, in the treatment of autoimmune disease.
methodsSynovial tissues from RA and osteoarthritis patients were analyzed for the expression of Bim and CD68 using immunohistochemistry. Macrophages from Bim(-/-) mice were examined for their response to lipopolysaccharide (LPS) using flow cytometry, real-time polymerase chain reaction analysis, enzyme-linked immunosorbent assay, and immunoblotting. Bim(-/-) mice were stimulated with thioglycollate or LPS and examined for macrophage activation and cytokine production. Experimental arthritis was induced using the K/BxN serum-transfer model. A mimetic peptide corresponding to the BH3 domain of Bim (TAT-BH3) was administered as a prophylactic agent and as a therapeutic agent. Edema of the ankles and histopathologic analysis of ankle tissue sections were used to determine the severity of arthritis, its cellular composition, and the degree of apoptosis.
resultsThe expression of Bim was reduced in RA synovial tissue as compared with controls, particularly in macrophages. Bim(-/-) macrophages displayed elevated expression of markers of inflammation and secreted more interleukin-1beta following stimulation with LPS or thioglycollate. TAT-BH3 ameliorated arthritis development, reduced the number of myeloid cells in the joint, and enhanced apoptosis without inducing cytotoxicity.
conclusionThese data demonstrate that BH3 mimetic therapy may have significant potential for the treatment of RA.
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Registered trials
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