ArticleInternational journal of molecular sciences2022
ZNF281 Promotes Colon Fibroblast Activation in TGFβ1-Induced Gut Fibrosis.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 16 citations in OpenAlex.
- A Large-Scale Method to Measure the Stoichiometries of Protein Poly-ADP-Ribosylation.ACS chemical biology · 2026Article
- Zinc finger proteins (ZFPs) in health and disease.Molecular biomedicine · 2026Review
- Developing a protocol to counteract spontaneous in vitro activation of intestinal fibroblasts using design of experiments.npj biomedical innovations · 2026Article
- Developing a Cell Culture Protocol to Induce Quiescence in Intestinal Fibroblasts Using Design of Experiments Statistical Optimization.Research square · 2025Article
- Cold, Hot, and Lethal-The Tumour Microenvironment and the Immunology of Head and Neck Squamous Cell Carcinoma.International journal of molecular sciences · 2025Review
- Single-cell and spatial transcriptomics profile the interaction ofTranslational lung cancer research · 2025Article
- Inflammation-fibrosis interplay in inflammatory bowel disease: mechanisms, progression, and therapeutic strategies.Frontiers in pharmacology · 2025Review
- Article
- Inhibition of intestinal inflammation and fibrosis by Scutellaria Baicalensis georgi and Boswellia serrata in human epithelial cells and fibroblasts.Immunity, inflammation and disease · 2024Article
- Mechanism of Action and Therapeutic Implications of Nrf2/HO-1 in Inflammatory Bowel Disease.Antioxidants (Basel, Switzerland) · 2024Review
- The Diagnosis of Intestinal Fibrosis in Crohn's Disease-Present and Future.International journal of molecular sciences · 2024Review
- tRF3-IleAAT reduced extracellular matrix synthesis in diabetic kidney disease mice by targeting ZNF281 and inhibiting ferroptosis.Acta pharmacologica Sinica · 2024Article
- Molecular targets associated with ulcerative colitis and the benefits of atractylenolides-based therapy.Frontiers in pharmacology · 2024Review
- The role of Nrf2 in the pathogenesis and treatment of ulcerative colitis.Frontiers in immunology · 2023Review
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Crohn's disease (CD) and ulcerative colitis (UC) are chronic inflammatory disorders of the gastrointestinal tract. Chronic inflammation is the main factor leading to intestinal fibrosis, resulting in recurrent stenosis, especially in CD patients. Currently, the underlying molecular mechanisms of fibrosis are still unclear. ZNF281 is a zinc-finger transcriptional regulator that has been characterized as an epithelial-to-mesenchymal transition (EMT)-inducing transcription factor, suggesting its involvement in the regulation of pluripotency, stemness, and cancer. The aim of this study is to investigate in vivo and in vitro the role of ZNF281 in intestinal fibrogenesis. Intestinal fibrosis was studied in vivo in C57BL/6J mice with chronic colitis induced by two or three cycles of administration of dextran sulfate sodium (DSS). The contribution of ZNF281 to gut fibrosis was studied in vitro in the human colon fibroblast cell line CCD-18Co, activated by the pro-fibrotic cytokine TGFβ1. ZNF281 was downregulated by siRNA transfection, and RNA-sequencing was performed to identify genes regulated by TGFβ1 in activated colon fibroblasts via ZNF281. Results showed a marked increase of ZNF281 in in vivo murine fibrotic colon as well as in in vitro human colon fibroblasts activated by TGFβ1. Moreover, abrogation of ZNF281 in TGFβ1-treated fibroblasts affected the expression of genes belonging to specific pathways linked to fibroblast activation and differentiation into myofibroblasts. We demonstrated that ZNF281 is a key regulator of colon fibroblast activation and myofibroblast differentiation upon fibrotic stimuli by transcriptionally controlling extracellular matrix (ECM) composition, remodeling, and cell contraction, highlighting a new role in the onset and progression of gut fibrosis.
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