ArticlePloS one2015
Tim-4 Inhibits NO Generation by Murine Macrophages.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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The trial behind it
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Who cites it
10 citing papers in PubMed, 21 citations in OpenAlex.
- Macrophage Tim-4 protects against deep vein thrombosis by binding CK2β to suppress inflammatory responses.Frontiers in immunology · 2025Article
- Article
- T-Cell Immunoglobulin and Mucin Domain-Containing Protein-4 Is Critical for Kupffer Cell Homeostatic Function in the Activation and Resolution of Liver Ischemia Reperfusion Injury.Hepatology (Baltimore, Md.) · 2021Article
- Management of cell death in parasitic infections.Seminars in immunopathology · 2021Review
- Novel Roles of the Tim Family in Immune Regulation and Autoimmune Diseases.Frontiers in immunology · 2021Review
- IL-6 promotes metastasis of non-small-cell lung cancer by up-regulating TIM-4 via NF-κB.Cell proliferation · 2020Article
- Tim-4 in Health and Disease: Friend or Foe?Frontiers in immunology · 2020Review
- Hepatic Ischemic Preconditioning Alleviates Ischemia-Reperfusion Injury by Decreasing TIM4 Expression.International journal of biological sciences · 2018Article
- Tim-4 protects mice against lipopolysaccharide-induced endotoxic shock by suppressing the NF-κB signaling pathway.Laboratory investigation; a journal of technical methods and pathology · 2016Article
- TIM-4 promotes the growth of non-small-cell lung cancer in a RGD motif-dependent manner.British journal of cancer · 2015Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveT cell immunoglobulin- and mucin-domain-containing molecule-4 (Tim-4) receives much attention as a potentially negative regulator of immune responses. However, its modulation on macrophages has not been fully elucidated so far. This study aimed to identify the role of Tim-4 in nitric oxide (NO) modulation.
methodsMacrophages were stimulated with 100 ng/ml LPS or 100 U/ml IFN-γ. RT-PCR was performed to detect TIM-4 mRNA expression. Tim-4 blocking antibody and NF-κB inhibitory ligand were involved in the study. NO levels were assayed by Griess reaction. Phosphorylation of NF-κB, Jak2 or Stat1 was verified by western blot.
resultsTim-4 was up-regulated in murine macrophages after interferon-gamma (IFN-γ) stimulation. Tim-4 over-expression decreased NO production and inducible nitric oxide synthase (iNOS) expression in lipopolysaccharide (LPS) or IFN-γ-stimulated macrophages. Consistently, Tim-4 blockade promoted LPS or IFN-γ-induced NO secretion and iNOS expression. Tim-4 over-expression decreased LPS-induced nuclear factor kappa B (NF-κB) p65 phosphorylation in macrophages, which was abrogated by NF-κB inhibitory ligand. On the contrary, Tim-4 blocking increased LPS-induced NF-κB signaling, which was also abrogated by NF-κB inhibition. In addition, Tim-4 blockade promoted Jak2 and Stat1 phosphorylation in IFN-γ stimulated macrophages.
conclusionThese results indicate that Tim-4 is involved in negative regulation of NO production in macrophages, suggesting the critical role of Tim-4 in immune related diseases.
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