ArticleJournal of gastroenterology2015
Par-3 modulates intestinal epithelial barrier function through regulating intracellular trafficking of occludin and myosin light chain phosphorylation.
Article in Journal of gastroenterology, 2015. 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, 26 citations in OpenAlex.
- The Serine Protease-Serine Protease Inhibitor Regulatory Network in Inflammatory Bowel Disease: From Molecular Mechanisms to Novel Therapeutic Horizons.Journal of advanced research · 2026Review
- Glucocorticoid receptor-mediatediScience · 2023Article
- Insights of Endocytosis Signaling in Health and Disease.International journal of molecular sciences · 2023Review
- Article
- Extracellular Vesicles in Human Milk.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Endocytosis of Intestinal Tight Junction Proteins: In Time and Space.Inflammatory bowel diseases · 2021Review
- Intestinal epithelial cells related lncRNA and mRNA expression profiles in dextran sulphate sodium-induced colitis.Journal of cellular and molecular medicine · 2021Article
- Otic Neurogenesis inFrontiers in neuroanatomy · 2021Article
- Aryl Hydrocarbon Receptor Activation Modulates Intestinal Epithelial Barrier Function by Maintaining Tight Junction Integrity.International journal of biological sciences · 2018Article
- Disruption of the epithelial barrier during intestinal inflammation: Quest for new molecules and mechanisms.Biochimica et biophysica acta. Molecular cell research · 2017Review
- Article
- Inflammation and the Intestinal Barrier: Leukocyte-Epithelial Cell Interactions, Cell Junction Remodeling, and Mucosal Repair.Gastroenterology · 2016Review
- Ameliorative effect of melatonin against increased intestinal permeability in diabetic rats: possible involvement of MLCK-dependent MLC phosphorylation.Molecular and cellular biochemistry · 2016Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTight junctions play a critical role in the maintenance of intestinal barrier function. Partitioning-defective protein 3 (Par-3) can regulate intestinal barrier function through the modulation of tight junction assembly and cell polarity. However, the mechanisms are still not fully understood.
methodsAdult C57BL/6 mice were treated with dextran sulfate sodium for 7 days, and segments of colon were harvested for immunofluorescent staining of Par-3. Caco-2 intestinal epithelial cells were treated with tumor necrosis factor α (TNF-α) for 24 h, and Par-3 expression was detected by Western blot analysis and immunofluorescence. Additionally, Caco-2 cells were treated with Par-3 small interfering RNA, and altered expression and subcellular localization of tight junction proteins were studied by Western blot analysis and immunofluorescence. Furthermore, the interaction between Par-3 and myosin light chain (MLC) was detected by immunoprecipitation.
resultsPar-3 was downregulated in murine dextran sulfate sodium induced acute inflammation and TNF-α-treated Caco-2 cells. Depletion of Par-3 expression by small interfering RNA delayed intestinal epithelial barrier development in Caco-2 cells. This regulation was due to the redistribution of the tight junction protein occludin rather than the altered total levels of tight junction proteins. Par-3 silencing blocked the trafficking of occludin from or through the Golgi complex to the cell surface, and dramatically induced occludin accumulated at the Golgi complex. Importantly, Par-3 can interact with MLC, and loss of Par-3 upregulated MLC kinase expression and MLC phosphorylation, which contributed to intestinal epithelial barrier dysfunction.
conclusionsThese results indicate that Par-3 plays an important role in the modulation of intestinal barrier function by regulating delivery of occludin as well as suppression of MLC phosphorylation.
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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.