ArticleArthritis research & therapy2020
Tumour necrosis factor alpha promotes secretion of 14-3-3η by inducing necroptosis in macrophages.
Article in Arthritis research & therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 41 citations in OpenAlex.
- Pivotal contribution of super-enhancer-driven KLF6 expression to the adipogenesis of human adipose-derived stem cells.Inflammation and regeneration · 2026Article
- Biomarkers of treatment response in rheumatoid arthritis: from conventional markers to tissue immunophenotype.Frontiers in immunology · 2026Review
- Frontier research on mechanisms of bone destruction in rheumatoid arthritis.Frontiers in cell and developmental biology · 2026Review
- Dysregulation of Different Modes of Programmed Cell Death in Rheumatoid Arthritis Fibroblast-Like Synoviocyte.International journal of rheumatic diseases · 2025Review
- Understanding the role of 14-3-3Ƞ protein in rheumatoid arthritis: from molecular dysregulation to therapeutic Redirection.Molecular biology reports · 2025Review
- Critical roles of IL-6 signaling in myoblast differentiation of human adipose-derived mesenchymal stem cells.Inflammation and regeneration · 2025Article
- Mechanistic and therapeutic insights into the function of different cell death modalities in rheumatoid arthritis: emphasis on the crosstalk with non-coding RNAs.Frontiers in immunology · 2025Review
- Programmed Cell Death in Rheumatoid Arthritis.Journal of inflammation research · 2025Review
- Versatility of 14-3-3 proteins and their roles in bone and joint-related diseases.Bone research · 2024Review
- Identification of necroptosis-related genes in ankylosing spondylitis by bioinformatics and experimental validation.Journal of cellular and molecular medicine · 2024Article
- Downregulation of BIRC2 hinders the progression of rheumatoid arthritis through regulating TRADD.Immunity, inflammation and disease · 2023Article
- Tailored therapeutic decision of rheumatoid arthritis using proteomic strategies: how to start and when to stop?Clinical proteomics · 2023Review
- IL-6 production through repression of UBASH3A gene via epigenetic dysregulation of super-enhancer in CD4Inflammation and regeneration · 2022Article
- Article
- 14-3-3η Promotes Invadosome Formation via the FOXO3-Snail Axis in Rheumatoid Arthritis Fibroblast-like Synoviocytes.International journal of molecular sciences · 2021Article
- Cell-Free DNA in Rheumatoid Arthritis.International journal of molecular sciences · 2021Review
- Citrullinated Histone H3 Mediates Sepsis-Induced Lung Injury Through Activating Caspase-1 Dependent Inflammasome Pathway.Frontiers in immunology · 2021Article
- Apoptosis, Autophagy, NETosis, Necroptosis, and Pyroptosis Mediated Programmed Cell Death as Targets for Innovative Therapy in Rheumatoid Arthritis.Frontiers in immunology · 2021Review
- Article
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background14-3-3η is an intracellular protein also detected in the serum and synovial fluid of patients with rheumatoid arthritis (RA). It is closely related to disease activity and anti-cyclic citrullinated peptide antibody levels. However, the main source of 14-3-3η and the mechanism of its release into the extracellular space remain unclear. Addressing these two points was the main goal of the current study.
methodsThe source of 14-3-3η was investigated by immunostaining RA synovial tissue. Fibroblast-like synoviocytes, CD4
resultsMacrophages from the synovial tissue from RA, but not osteoarthritis, showed dense and widespread cytoplasmic staining for the 14-3-3η protein, co-localized with peptidylarginine deiminase 4. Swelling and membrane rupture of macrophages were induced by treatment with TNF-α, but not interleukin (IL) 6/soluble IL-6 receptor (sIL-6R). Increased MLKL phosphorylation followed by necroptosis was also induced in TNF-α-stimulated macrophages. Necrostatin-1, a necroptosis inhibitor, antagonized MLKL phosphorylation. High levels of 14-3-3η were detected in the culture supernatants of macrophages stimulated with diamide and TNF-α, but not IL-6/sIL-6R.
conclusionsMacrophages that highly express 14-3-3η undergo TNF-α-induced necroptosis with damage to the cellular structure, resulting in the secretion of 14-3-3η into the extracellular space. The current study provides a novel mechanism for 14-3-3η level increase in the RA synovial fluid.
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