ArticleProceedings of the National Academy of Sciences of the United States of America2016
Enhanced stability of tristetraprolin mRNA protects mice against immune-mediated inflammatory pathologies.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed.
- Improving Dietary Intake of Essential Nutrients Can Ameliorate Inflammation in Patients with Diabetic Foot Ulcers.Nutrients · 2022Trial
- The ZFP36 Family as Post-Transcriptional Regulators in Physiology and Disease.International journal of molecular sciences · 2026Review
- Endothelin-1 induces Zfp36 family RNA-binding proteins and restrains cytokine and chemokine production in reactive astrocytes.The Journal of biological chemistry · 2026Article
- RNA-binding proteins and ribonucleoproteins as determinants of immunity.Nature reviews. Immunology · 2026Review
- Tristetraprolin protects against ozone-induced acute lung injury and inflammation in mice.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- The ZFP36-FTO axis is a key regulator of macrophage activation and a druggable therapeutic target of sepsis.iScience · 2025Article
- Myeloid-specific tristetraprolin mitigates postsurgical incisional pain by suppressing proinflammatory responses.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- Differential Regulation of TCR-Induced ZFP36 and ZFP36L1 Expression by Cyclosporin A in CD8European journal of immunology · 2025Article
- Myeloid-specific Tristetraprolin mitigates postsurgical incisional pain by suppressing proinflammatory responses.Research square · 2025Article
- Article
- Tristetraprolin regulates the skeletal phenotype and osteoclastogenic potential through monocytic myeloid-derived suppressor cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Synergistic roles of tristetraprolin family members in myeloid cells in the control of inflammation.Life science alliance · 2024Article
- ZFP36-mediated mRNA decay regulates metabolism.Cell reports · 2023Article
- The nexus between RNA-binding proteins and their effectors.Nature reviews. Genetics · 2023Review
- Clinical implications of tristetraprolin (TTP) modulation in the treatment of inflammatory diseases.Pharmacology & therapeutics · 2022Review
- The ZFP36 family of RNA binding proteins regulates homeostatic and autoreactive T cell responses.Science immunology · 2022Article
- Beta-hydroxybutyrate dampens adipose progenitors' profibrotic activation through canonical Tgfβ signaling and non-canonical ZFP36-dependent mechanisms.Molecular metabolism · 2022Article
- ZFP36L1 Regulates Fgf21 mRNA Turnover and Modulates Alcoholic Hepatic Steatosis and Inflammation in Mice.The American journal of pathology · 2022Article
- Tristetraprolin limits age-related expansion of myeloid-derived suppressor cells.Frontiers in immunology · 2022Article
- Targeting Zinc Finger Proteins with Exogenous Metals and Molecules: Lessons learned from Tristetraprolin, a CCCH type Zinc Finger.European journal of inorganic chemistry · 2021Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Tristetraprolin (TTP) is an inducible, tandem zinc-finger mRNA binding protein that binds to adenylate-uridylate-rich elements (AREs) in the 3'-untranslated regions (3'UTRs) of specific mRNAs, such as that encoding TNF, and increases their rates of deadenylation and turnover. Stabilization of Tnf mRNA and other cytokine transcripts in TTP-deficient mice results in the development of a profound, chronic inflammatory syndrome characterized by polyarticular arthritis, dermatitis, myeloid hyperplasia, and autoimmunity. To address the hypothesis that increasing endogenous levels of TTP in an intact animal might be beneficial in the treatment of inflammatory diseases, we generated a mouse model (TTPΔARE) in which a 136-base instability motif in the 3'UTR of TTP mRNA was deleted in the endogenous genetic locus. These mice appeared normal, but cultured fibroblasts and macrophages derived from them exhibited increased stability of the otherwise highly labile TTP mRNA. This resulted in increased TTP protein expression in LPS-stimulated macrophages and increased levels of TTP protein in mouse tissues. TTPΔARE mice were protected from collagen antibody-induced arthritis, exhibited significantly reduced inflammation in imiquimod-induced dermatitis, and were resistant to induction of experimental autoimmune encephalomyelitis, presumably by dampening the excessive production of proinflammatory mediators in all cases. These data suggest that increased systemic levels of TTP, secondary to increased stability of its mRNA throughout the body, can be protective against inflammatory disease in certain models and might be viewed as an attractive therapeutic target for the treatment of human inflammatory diseases.
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