ArticleJournal of immunology (Baltimore, Md. : 1950)2010
Genetic sphingosine kinase 1 deficiency significantly decreases synovial inflammation and joint erosions in murine TNF-alpha-induced arthritis.
Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.
What it found
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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
52 citing papers in PubMed, 1 synthesis or guideline pooled it, 90 citations in OpenAlex.
- Efferocytosis and inflammation: a bibliometric and systematic analysis.Frontiers in medicine · 2025Pooled it
- Epigenetic silencing of SPHK1-IRF7 axis drives inflammaging in age-related meniscus degeneration via sphingolipid-immune dysregulation.Journal of orthopaedic surgery and research · 2025Article
- Investigating the underlying mechanisms of the ethanol extract of saussureae involucratae herba in anti-rheumatoid arthritis effect based on sphingolipidomics.Frontiers in pharmacology · 2025Article
- Signaling controversy and future therapeutical perspectives of targeting sphingolipid network in cancer immune editing and resistance to tumor necrosis factor-α immunotherapy.Cell communication and signaling : CCS · 2024Review
- Apoptotic cell clearance components in inflammatory arthritis.Immunological reviews · 2023Review
- The Ying and Yang of Sphingosine-1-Phosphate Signalling within the Bone.International journal of molecular sciences · 2023Review
- Article
- Single-cell multimodal analysis identifies common regulatory programs in synovial fibroblasts of rheumatoid arthritis patients and modeled TNF-driven arthritis.Genome medicine · 2022Article
- Indigenous Nigeria medicinal herbal remedies: A potential source for therapeutic against rheumatoid arthritis.Experimental biology and medicine (Maywood, N.J.) · 2022Review
- Sphingosine 1-phosphate receptor-targeted therapeutics in rheumatic diseases.Nature reviews. Rheumatology · 2022Review
- Parathyroid hormone signaling in mature osteoblasts/osteocytes protects mice from age-related bone loss.Aging · 2021Article
- Targeting S1PRs as a Therapeutic Strategy for Inflammatory Bone Loss Diseases-Beyond Regulating S1P Signaling.International journal of molecular sciences · 2021Review
- Bioactive sphingolipids: Advancements and contributions from the laboratory of Dr. Lina M. Obeid.Cellular signalling · 2021Review
- The Role of Sphingolipid Metabolism in Bone Remodeling.Frontiers in cell and developmental biology · 2021Review
- Sphingosine-1-phosphate in anti-neutrophil cytoplasmic antibody-associated vasculitis: coagulation-related clinical indicators and complications.Bioscience reports · 2020Observational
- Article
- Sphingosine-1-Phosphate and Macrophage Biology-How the Sphinx Tames the Big Eater.Frontiers in immunology · 2019Review
- S1P-S1PR1 Signaling: the "Sphinx" in Osteoimmunology.Frontiers in immunology · 2019Review
- Effects of extracorporeal shock waves on neuralgia in diabetic rats.Journal of pain research · 2019Article
- SPHK-2 Promotes the Particle-Induced Inflammation of RAW264.7 by Maintaining Consistent Expression of TNF-α and IL-6.Inflammation · 2018Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Sphingosine kinase 1 (SphK1) is an enzyme that converts sphingosine to bioactive sphingosine-1-phosphate. Recent in vitro data suggest a potential role of SphK1 in TNF-alpha-mediated inflammation. Our aims in this study were to determine the in vivo significance of SphK1 in TNF-alpha-mediated chronic inflammation and to define which pathogenic mechanisms induced by TNF-alpha are SphK1 dependent. To pursue these aims, we studied the effect of SphK1 deficiency in an in vivo model of TNF-alpha-induced chronic inflammatory arthritis. Transgenic hTNF-alpha mice, which develop spontaneous inflammatory erosive arthritis beginning at 14-16 wk, were crossed with SphK1 null mice (SphK1(-/-)), on the C57BL6 genetic background. Beginning at 4 mo of age, hTNF/SphK1(-/-) mice had significantly less severe clinically evident paw swelling and deformity, less synovial and periarticular inflammation, and markedly decreased bone erosions as measured quantitatively through micro-CT images. Mechanistically, the mice lacking SphK1 had less articular cyclooxygenase 2 protein and fewer synovial Th17 cells than did hTNF/SphK1(+/+) littermates. Microarray analysis and real-time RT-PCR of the ankle synovial tissue demonstrated that hTNF/SphK1(-/-) mice had increased transcript levels of suppressor of cytokine signaling 3 compared with hTNF/SphK1(+/+) mice, likely also contributing to the decreased inflammation in the SphK1-deficient mice. Finally, significantly fewer mature osteoclasts were detected in the ankle joints of hTNF/SphK1(-/-) mice compared with hTNF/SphK1(+/+) mice. These data indicate that SphK1 plays a key role in hTNF-alpha-induced inflammatory arthritis via impacting synovial inflammation and osteoclast number.
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Registered trials
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.