ArticleJCI insight2021
TTP protects against acute liver failure by regulating CCL2 and CCL5 through m6A RNA methylation.
Article in JCI insight, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 31 citations in OpenAlex.
- Tristetraprolin attenuates schistosomiasis-induced liver fibrosis through m⁶A-mediated regulation of TGF-β1 mRNA stability.PLoS pathogens · 2026Article
- The protective effects and mechanism of myricetin in liver diseases (Review).Molecular medicine reports · 2025Review
- Histone demethylases in autophagy and inflammation.Cell communication and signaling : CCS · 2025Review
- Molecular Insights into RNA Modifications and Their Role in Shaping Immune Responses and Tumor Microenvironments.Current gene therapy · 2025Review
- Innate immune activation in vitiligo: mechanisms and pathophysiological implications.Frontiers in immunology · 2025Review
- m6A epitranscriptomic modification in hepatocellular carcinoma: implications for the tumor microenvironment and immunotherapy.Frontiers in immunology · 2025Review
- Unraveling the landscape of m6A RNA methylation in wound healing and scars.Cell death discovery · 2024Review
- KHSRP ameliorates acute liver failure by regulating pre-mRNA splicing through its interaction with SF3B1.Cell death & disease · 2024Article
- The evolving process of ferroptosis in thyroid cancer: Novel mechanisms and opportunities.Journal of cellular and molecular medicine · 2024Review
- Microglia in retinal angiogenesis and diabetic retinopathy.Angiogenesis · 2024Review
- Adipocyte-Specific Hnrnpa1 Knockout Aggravates Obesity-Induced Metabolic Dysfunction via Upregulation of CCL2.Diabetes · 2024Article
- Decoding mGenes & diseases · 2024Review
- The m6A methyltransferase METTL16 negatively regulates MCP1 expression in mesenchymal stem cells during monocyte recruitment.JCI insight · 2023Article
- Insights into the role of nucleotide methylation in metabolic-associated fatty liver disease.Frontiers in immunology · 2023Review
- miR-182-5p attenuatesActa biochimica et biophysica Sinica · 2022Article
- Transplanted allogeneic cardiac progenitor cells secrete GDF-15 and stimulate an active immune remodeling process in the ischemic myocardium.Journal of translational medicine · 2022Article
- The RNA-binding protein IMP2 drives a stromal-Th17 cell circuit in autoimmune neuroinflammation.JCI insight · 2022Article
- Tristetraprolin limits age-related expansion of myeloid-derived suppressor cells.Frontiers in immunology · 2022Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tristetraprolin (TTP), an important immunosuppressive protein regulating mRNA decay through recognition of the AU-rich elements (AREs) within the 3'-UTRs of mRNAs, participates in the pathogenesis of liver diseases. However, whether TTP regulates mRNA stability through other mechanisms remains poorly understood. Here, we report that TTP was upregulated in acute liver failure (ALF), resulting in decreased mRNA stabilities of CCL2 and CCL5 through promotion of N6-methyladenosine (m6A) mRNA methylation. Overexpression of TTP could markedly ameliorate hepatic injury in vivo. TTP regulated the mRNA stabilization of CCL2 and CCL5. Interestingly, increased m6A methylation in CCL2 and CCL5 mRNAs promoted TTP-mediated RNA destabilization. Moreover, induction of TTP upregulated expression levels of WT1 associated protein, methyltransferase like 14, and YT521-B homology N6-methyladenosine RNA binding protein 2, which encode enzymes regulating m6A methylation, resulting in a global increase of m6A methylation and amelioration of liver injury due to enhanced degradation of CCL2 and CCL5. These findings suggest a potentially novel mechanism by which TTP modulates mRNA stabilities of CCL2 and CCL5 through m6A RNA methylation, which is involved in the pathogenesis of ALF.
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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.