ArticleeLife2022
Macrophage inflammation resolution requires CPEB4-directed offsetting of mRNA degradation.
Article in eLife, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 23 citations in OpenAlex.
- RNA-binding proteins and ribonucleoproteins as determinants of immunity.Nature reviews. Immunology · 2026Review
- Stress-Induced Down-Regulation of CPEB4 Disrupts Sodium Channel Regulation and Myocardial Excitability.JACC. Basic to translational science · 2026Article
- Dynamic subtype- and context-specific subcellular RNA regulation in growth cones of developing neurons of the cerebral cortex.Nature neuroscience · 2026Article
- Cytoplasmic regulation of the poly(A) tail length as a potential therapeutic target.RNA (New York, N.Y.) · 2025Review
- Accurate isoform quantification by joint short- and long-read RNA-sequencing.bioRxiv : the preprint server for biology · 2024Article
- Knockdown of CPEB1 and CPEB4 Inhibits Scar Formation via Modulation of TAK1 and SMAD Signaling.Annals of dermatology · 2023Article
- CPEB and translational control by cytoplasmic polyadenylation: impact on synaptic plasticity, learning, and memory.Molecular psychiatry · 2023Review
- An intrinsically interpretable neural network architecture for sequence-to-function learning.Bioinformatics (Oxford, England) · 2023Article
- An intrinsically interpretable neural network architecture for sequence to function learning.bioRxiv : the preprint server for biology · 2023Article
- Epigenetic Regulation of Macrophage Polarization in Cardiovascular Diseases.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Classification of subtypes and identification of dysregulated genes in sepsis.Frontiers in cellular and infection microbiology · 2023Article
- Control of immediate early gene expression by CPEB4-repressor complex-mediated mRNA degradation.Genome biology · 2022Article
- Macrophage inflammation resolution requires CPEB4-directed offsetting of mRNA degradation.eLife · 2022Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic inflammation is a major cause of disease. Inflammation resolution is in part directed by the differential stability of mRNAs encoding pro-inflammatory and anti-inflammatory factors. In particular, tristetraprolin (TTP)-directed mRNA deadenylation destabilizes AU-rich element (ARE)-containing mRNAs. However, this mechanism alone cannot explain the variety of mRNA expression kinetics that are required to uncouple degradation of pro-inflammatory mRNAs from the sustained expression of anti-inflammatory mRNAs. Here, we show that the RNA-binding protein CPEB4 acts in an opposing manner to TTP in macrophages: it helps to stabilize anti-inflammatory transcripts harboring cytoplasmic polyadenylation elements (CPEs) and AREs in their 3'-UTRs, and it is required for the resolution of the lipopolysaccharide (LPS)-triggered inflammatory response. Coordination of CPEB4 and TTP activities is sequentially regulated through MAPK signaling. Accordingly, CPEB4 depletion in macrophages impairs inflammation resolution in an LPS-induced sepsis model. We propose that the counterbalancing actions of CPEB4 and TTP, as well as the distribution of CPEs and AREs in their target mRNAs, define transcript-specific decay patterns required for inflammation resolution. Thus, these two opposing mechanisms provide a fine-tuning control of inflammatory transcript destabilization while maintaining the expression of the negative feedback loops required for efficient inflammation resolution; disruption of this balance can lead to disease.
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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.