ArticleCell and tissue research2017
MCL-1 is modulated in Crohn's disease fibrosis by miR-29b via IL-6 and IL-8.
Article in Cell and tissue research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 35 citations in OpenAlex.
- Mcl1 as a Molecular Switch Linking Inflammatory Bowel Diseases to Colorectal Tumorigenesis.Biomolecules · 2026Review
- ceRNA Network Dynamics in Inflammatory Bowel Disease: The LncRNA-miRNA-mRNA Axis in Intestinal Homeostasis and Inflammation.Cell biochemistry and biophysics · 2026Review
- MicroRNA‑microbiome cross‑kingdom networks drive inflammatory bowel disease through dynamic regulatory ecosystems (Review).International journal of molecular medicine · 2026Review
- Molecular Basis of Chronic Intestinal Wall Fibrosis in Inflammatory Bowel Diseases.International journal of molecular sciences · 2025Review
- Intestinal fibrosis associated with inflammatory bowel disease: Known and unknown.Chinese medical journal · 2025Review
- Tipping the balance of cell death: alternative splicing as a source of MCL-1S in cancer.Cell death & disease · 2024Review
- Thyroid dysfunction in Hashimoto's thyroiditis: a pilot study on the putative role of miR-29a and TGFβ1.Endocrine · 2024Article
- Phytochemical Compounds as Promising Therapeutics for Intestinal Fibrosis in Inflammatory Bowel Disease: A Critical Review.Nutrients · 2024Review
- Aberrant miR-29 is a predictive feature of severe phenotypes in pediatric Crohn's disease.JCI insight · 2024Article
- Inflammation as a driver of hematological malignancies.Frontiers in oncology · 2024Review
- miRNA Molecules-Late Breaking Treatment for Inflammatory Bowel Diseases?International journal of molecular sciences · 2023Review
- miRNAs Can Affect Intestinal Epithelial Barrier in Inflammatory Bowel Disease.Frontiers in immunology · 2022Review
- Maintenance of gut barrier integrity after injury: Trust your gut microRNAs.Journal of leukocyte biology · 2021Review
- miR-452-5p regulates the responsiveness of intestinal epithelial cells in inflammatory bowel disease through Mcl-1.Experimental and therapeutic medicine · 2021Article
- The role of miR-29 family in disease.Journal of cellular biochemistry · 2021Review
- Noncoding RNAs as Promising Diagnostic Biomarkers and Therapeutic Targets in Intestinal Fibrosis of Crohn's Disease: The Path From Bench to Bedside.Inflammatory bowel diseases · 2021Review
- Intestinal mucosa-derived DNA methylation signatures in the penetrating intestinal mucosal lesions of Crohn's disease.Scientific reports · 2021Article
- MiR-155 promotes colitis-associated intestinal fibrosis by targeting HBP1/Wnt/β-catenin signalling pathway.Journal of cellular and molecular medicine · 2021Article
- Mechanism of fibrosis and stricture formation in Crohn's disease.Scandinavian journal of immunology · 2020Review
- MicroRNA Biomarkers in IBD-Differential Diagnosis and Prediction of Colitis-Associated Cancer.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The miR-29 family is involved in fibrosis in multiple organs, including the intestine where miR-29b facilitates TGF-β-mediated up-regulation of collagen in mucosal fibroblasts from Crohn's disease (CD) patients. Myeloid cell leukemia-1 (MCL-1), a member of the B-cell CLL/Lymphoma 2 (BCL-2) apoptosis family, is involved in liver fibrosis and is targeted by miR-29b via its 3'-UTR in cultured cell lines. We investigate the role of MCL-1 and miR-29b in primary intestinal fibroblasts and tissue from stricturing CD patients. Transfection of CD intestinal fibroblasts with pre-miR-29b resulted in a significant increase in the mRNA expression of MCL-1 isoforms [MCL-1Long (L)/Extra Short (ES) and MCL-1Short (S)], although MCL-1S was expressed at significantly lower levels. Western blotting predominantly detected the anti-apoptotic MCL-1L isoform, and immunofluorescence showed that staining was localised in discrete nuclear foci. Transfection with pre-miR-29b or anti-miR-29b resulted in a significant increase or decrease, respectively, in MCL-1L foci. CD fibroblasts treated with IL-6 and IL-8, inflammatory cytokines upstream of MCL-1, increased the total mass of MCL-1L-positive foci. Furthermore, transfection of intestinal fibroblasts with pre-miR-29b resulted in an increase in mRNA and protein levels of IL-6 and IL-8. Finally, immunohistochemistry showed reduced MCL-1 protein expression in fibrotic CD samples compared to non-stricturing controls. Together, our findings suggest that induction of MCL-1 by IL-6/IL-8 may surmount any direct down-regulation by miR-29b via its 3'-UTR. We propose that an anti-fibrotic miR-29b/IL-6 IL-8/MCL-1L axis may influence intestinal fibrosis in CD. In the future, therapeutic modulation of this pathway might contribute to the management of fibrosis in CD.
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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.