ArticleInternational journal of molecular sciences2024
Anti-Inflammatory Effects of miR-369-3p via PDE4B in Intestinal Inflammatory Response.
Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- miR-369-3p Modulates LRRK2-Mediated Inflammation and Autophagy in RAW264.7 Macrophages.International journal of molecular sciences · 2026Article
- Mechanistic study of miR‑369‑3p in regulating the Wnt/β‑catenin signaling pathway via targeting SPTBN1 in inflammatory response and bone destruction of rheumatoid arthritis.Molecular medicine reports · 2026Article
- Identification and Validation of Key Purine Metabolism-Related Genes in Ulcerative Colitis Using Bioinformatics and Machine Learning.Journal of inflammation research · 2026Article
- Small RNA Profiles of Serum-Derived Extracellular Vesicles in the Comorbid Condition of Frailty and Obstructive Pulmonary Disease: An Observational, Cross-Sectional Study.Biomolecules · 2025Observational
- Article
- Targeting Phosphodiesterase 4 in Gastrointestinal and Liver Diseases: From Isoform-Specific Mechanisms to Precision Therapeutics.Biomedicines · 2025Review
- miR-369-3p Ameliorates Inflammation and Apoptosis in Intestinal Epithelial Cells via the MEK/ERK Signaling Pathway.International journal of molecular sciences · 2025Article
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Authors and funding
6 authors.
Funding
Abstract
Cyclic nucleotide phosphodiesterases (PDEs) consist of a family of enzymes expressed in several types of cells, including inflammatory cells, that play a pivotal role in inflammation. Several studies have demonstrated that the inhibition of PDE4 results in a reduced inflammatory response via PKA and CREB signaling. Hence, PDE4 suppression improves the inflammatory feedback typical of several diseases, such as inflammatory bowel disease (IBD). In our previous studies, we have demonstrated that miR-369-3p regulates inflammatory responses, modulating different aspects of the inflammatory process. The aim of this study was to demonstrate an additional anti-inflammatory effect of miR-369-3p targeting PDE4B, one of the widely expressed isoforms in immune cells. We found that miR-369-3p was able to reduce the expression of PDE4B, elevating the intracellular levels of cAMP. This accumulation increased the expression of PKA and pCREB, mitigating the release of pro-inflammatory cytokines and promoting the release of anti-inflammatory cytokines. To prove that PDE4B is a good therapeutic target in IBD, we also demonstrate that the expression of PDE4B was increased in UC patients compared to healthy controls, affecting the immune infiltrate. PDE4B is considered an important player in inflammatory progression; hence, our results show the ability of miR-369-3p to ameliorate inflammation by targeting PDE4B, supporting its future application as a new therapeutic approach in IBD.
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Registered trials
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