ArticlePloS one2021
Matrix Metalloproteinase-9 (MMP-9) induced disruption of intestinal epithelial tight junction barrier is mediated by NF-κB activation.
Article in PloS one, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 84 citations in OpenAlex.
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- KDM3A drives NSCLC proliferation and metastasis via H3K9 demethylation, EMT activation and MMP-9 upregulation.Biomolecules & biomedicine · 2025Article
- Candida albicans Enhances Protease Activity and Activates MyD88-Dependent IL-1β Production in Human Keratinocytes.Mycoses · 2025Article
- Key Common Genes with LTF and MMP9 Between Sepsis and Relapsed B-Cell Lineage Acute Lymphoblastic Leukemia in Children.Biomedicines · 2025Article
- The function of metalloproteinases in pathophysiology of inflammatory bowel disease and colon cancer.Journal of leukocyte biology · 2025Review
- NF-κB in inflammation and cancer.Cellular & molecular immunology · 2025Review
- Matrix Dynamics and Microbiome Crosstalk: Matrix Metalloproteinases as Key Players in Disease and Therapy.International journal of molecular sciences · 2025Review
- Quantitative profiling of the vaginal microbiota improves resolution of the microbiota-immune axis.Microbiome · 2025Article
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- Review
- Probiotics and the intestinal tight junction barrier function.Frontiers in cell and developmental biology · 2025Review
- The Improvement of Intestinal Mucosal Epithelial Barrier Integrity by 1,3,4-Oxadiazole Derivatives of Pyrrolo[3,4-Journal of inflammation research · 2025Article
- Clinical association and potential molecular mechanisms of neonatal sepsis and necrotizing enterocolitis.Frontiers in molecular biosciences · 2025Article
- Review
- The role of intestinal macrophage polarization in colitis-associated colon cancer.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundMatrix Metalloproteinase-9 (MMP-9) has been shown to play a key role in mediating inflammation and tissue damage in inflammatory bowel disease (IBD). In patients with IBD, the intestinal tight junction (TJ) barrier is compromised as characterized by an increase in intestinal permeability. MMP-9 is elevated in intestinal tissue, serum and stool of patients with IBD. Previous studies from our laboratory showed that MMP-9 causes an increase in intestinal epithelial TJ permeability and that the MMP-9 induced increase in intestinal permeability is an important pathogenic factor contributing to the development of intestinal inflammation in IBD. However, the intracellular mechanisms that mediate the MMP-9 modulation of intestinal barrier function remain unclear.
aimsThe main aim of this study was to further elucidate the molecular mechanisms involved in MMP-9 induced increase in intestinal epithelial TJ permeability using Caco-2 monolayers as an in-vitro model system.
resultsMMP-9 induced increase in Caco-2 TJ permeability was associated with activation and cytoplasmic-to-nuclear translocation of NF-κB p65. Knocking-down NF-κB p65 by siRNA transfection prevented the MMP-9 induced expression of the NF-κB target gene IL-8, myosin light chain kinase (MLCK) protein expression, and subsequently prevented the increase in Caco-2 TJ permeability. In addition, the effect of MMP-9 on Caco-2 intestinal epithelial TJ barrier function was not mediated by apoptosis or necrosis.
conclusionOur data show that the MMP-9 induced disruption of Caco-2 intestinal epithelial TJ barrier function is regulated by NF-κB pathway activation of MLCK.
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Registered trials
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