ArticleEMBO molecular medicine2012
Enterocyte STAT5 promotes mucosal wound healing via suppression of myosin light chain kinase-mediated loss of barrier function and inflammation.
Article in EMBO molecular medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
51 citing papers in PubMed, 81 citations in OpenAlex.
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- Tetrameric STAT5 regulates the formation of immune niche cells to protect stem cell regenerative repair against mucosal inflammation.Experimental & molecular medicine · 2026Article
- Gut microbiota-derived metabolites and IL-22 signaling in inflammatory bowel disease: context-dependent regulation of mucosal repair and inflammation.Frontiers in immunology · 2026Review
- Development of Nanocarrier-Based Oral Pegfilgrastim Formulations for Mitigating Hematopoietic Acute Radiation Syndrome.Advanced functional materials · 2025Article
- Therapeutic potential of Janus kinase inhibitors for the management of fibrosis in inflammatory bowel disease.Journal of Crohn's & colitis · 2025Review
- Strategies for targeting cytokines in inflammatory bowel disease.Nature reviews. Immunology · 2024Review
- Non-pituitary growth hormone enables colon cell senescence evasion.Aging cell · 2024Article
- Resveratrol Alleviates Zearalenone-Induced Intestinal Dysfunction in Mice through the NF-κB/Nrf2/HO-1 Signalling Pathway.Foods (Basel, Switzerland) · 2024Article
- Predictors of Efficacy of Janus Kinase Inhibitors in Patients Affected by Ulcerative Colitis.Journal of clinical medicine · 2024Review
- Ferroptosis: a new mechanism of traditional Chinese medicine for treating ulcerative colitis.Frontiers in pharmacology · 2024Review
- Monogenic deficiency in murine intestinal Cdc42 leads to mucosal inflammation that induces crypt dysplasia.Genes & diseases · 2024Article
- Non-pituitary GH regulation of the tissue microenvironment.Endocrine-related cancer · 2023Article
- Tetramerization of STAT5 regulates monocyte differentiation and the dextran sulfate sodium-induced colitis in mice.Frontiers in immunology · 2023Article
- Artificial Intelligence Analysis of Celiac Disease Using an Autoimmune Discovery Transcriptomic Panel Highlighted Pathogenic Genes including BTLA.Healthcare (Basel, Switzerland) · 2022Article
- Mechanisms of mucosal healing: treating inflammatory bowel disease without immunosuppression?Nature reviews. Gastroenterology & hepatology · 2022Review
- Challenges and opportunities targeting mechanisms of epithelial injury and recovery in acute intestinal graft-versus-host disease.Mucosal immunology · 2022Review
- Epithelial wound healing in inflammatory bowel diseases: the next therapeutic frontier.Translational research : the journal of laboratory and clinical medicine · 2021Review
- Targeting JAK/STAT signaling pathways in treatment of inflammatory bowel disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021Review
- Review
- Gene-Metabolite Network Linked to Inhibited Bioenergetics in Association With Spaceflight-Induced Loss of Male Mouse Quadriceps Muscle.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2020Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
Abstract
Epithelial myosin light chain kinase (MLCK)-dependent barrier dysfunction contributes to the pathogenesis of inflammatory bowel diseases (IBD). We reported that epithelial GM-CSF-STAT5 signalling is essential for intestinal homeostatic response to gut injury. However, mechanism, redundancy by STAT5 or cell types involved remained foggy. We here generated intestinal epithelial cell (IEC)-specific STAT5 knockout mice, these mice exhibited a delayed mucosal wound healing and dysfunctional intestinal barrier characterized by elevated levels of NF-κB activation and MLCK, and a reduction of zonula occludens expression in IECs. Deletion of MLCK restored intestinal barrier function in STAT5 knockout mice, and facilitated mucosal wound healing. Consistently, knockdown of stat5 in IEC monolayers led to increased NF-κB DNA binding to MLCK promoter, myosin light chain phosphorylation and tight junction (TJ) permeability, which were potentiated by administration of tumour necrosis factor-α (TNF-α), and prevented by concurrent NF-κB knockdown. Collectively, enterocyte STAT5 signalling protects against TJ barrier dysfunction and promotes intestinal mucosal wound healing via an interaction with NF-κB to suppress MLCK. Targeting IEC STAT5 signalling may be a novel therapeutic approach for treating intestinal barrier dysfunction in IBD.
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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.